Please review the rubric to ensure that your response meets the criteria. please use updated reference for each peer response respond to #1 K Mc. MondayMay 17 at 12:52pm Module 2 Discussion: Health History What strategies would you employ to obtain a complete health history? There are 3 things that I would do to complete a health history on a patient who was not able to provide answers. Interrogation of the patient’s representative. Clinical evaluation. Analysis of laboratory tests. First, by speaking with the patient’s representative, it would allow me to get the “back story” and understand the overall situation that is at hand. Most cases, it would be a family member of some sort that would be the go-to person. The family may be a potential source of information about a patient’s medical history when the patient is unsure or unable to answer questions regarding their medical history. This information can generally be regarded as accurate, but you may have similar issues with the patient’s family regarding health literacy and understanding (Nichol, 2020).
Secondly, by completing the clinical evaluation or a patient assessment. An organized assessment is the starting point for diagnostic reasoning. Because all health diagnoses, decisions, and treatments are based on the date you gather during the assessment, it is crucial be factual and complete (Jarvis et al., 2020). Lastly, laboratory value should ideally be evaluated in a manner consistent with the main goals of a health system. Laboratory values are required for many reasons which include disease prevention, early detection, establishing an accurate diagnosis, selecting the right treatment, avoiding delays in treatment, facilitating recovery, reducing disability, preventing relapse, or delaying disease progression and reducing the need for long term care (Sikaris, 2017). Provide a rationale for why you think these strategies would be effective. The interrogation must be carried out with the purpose of knowing a medical history (any illness or medical treatment). The clinical evaluation is carried out for the probable diagnosis of any pathology present in the patient, to determine the medical examinations to request. The analysis of laboratory tests are necessary to definitively diagnose the patient. References: Jarvis, C., Eckhardt, A.,
A patient with a chronic pain
This essay will discuss the mechanisms of chronic pain and how it relates to the patient. The focus of this essay will be on the pathophysiology of chronic pain. Chronic pain management, psychological, sociological and public health issues will also be discussed. Section A Mrs HR a 50 year old female who works as European Sales Manager for a large IT company presented to Royal South Hants Hospital Pain Clinic with worsening neck pain. HR has a constant severe and intense ache in right side of her neck with spasms in her right trapezius muscle. The pain is neither exacerbated nor relieved when pressure is applied. She has general background pain, aching and fatigue. HR’s pain is made worse by sitting or standing in an upright position for a prolonged period of time (>2hours), vibrations from driving, prolonged movement/exercise and stress at work. Her pain can vary considerably throughout the day and often keeps her awake at night. Her pain is improved by lying flat and medication. An MRI scan excluded any significant pathology or cord compression. She has general wear and tear of her neck muscles. Mrs HR has been seen by an orthopaedic surgeon, a pain clinic consultant, her GP, and a physiotherapist. Subjectively on a pain scale, the worst pain during an acute episode is 10/10, and the least pain experienced day to day is 3/10. On average the pain she experiences is 7/10. In 1995 HR injured her neck in a swimming pool, when someone jumping in landed on top of her. In 1997 HR suffered whiplash following a road traffic accident. At the time of the incidents HR experienced minimal discomfort. However, in 2005 the pain started to become a burden to her. Since 2005 the pain has gradually increased in intensity and frequency and she has general achiness/stiffness. In the past she has suffered from fibroids and migraines. She is allergic to tramadol which causes vomiting, excessive sweating and an increased heart rate. She has no significant family history and her systems review was unremarkable. On examination her reflexes, sensitivity, power and tone and coordination were unremarkable. HR is diagnosed as having nociceptive/inflammatory chronic pain due to previous damage to her deep neck muscles. The patient may also have some neuropathic pain but this has not been confirmed. She has completed pain questionnaires, including the McGill questionnaire. Previous to her pain clinic appointment her medications included; gabapentin 300mg tds po, co-codamol 30/500 qds po and robaxin 750mg prn (during an acute episode, approximately twice a month). These were changed to; gabapentin 300mg qds po, dihydrocodeine 60mg bd modified-release po and nortriptyline 25mg nocte po. HR experiences constipation as a side effect of co-codamol. HR uses a TENS machine at home, she has a hydrotherapy pool and spa at home that helps her relax. Mrs HR has lived with her husband, a barrister for 33 years. Her husband is understanding about her condition and would like her to give up her stressful job. However, HR enjoys her job, claiming that it makes her happy. They have no known financial constraints and are not taking or have previously taken any legal action in relation to Mrs HR pain. HR is a non-smoker and does not drink alcohol. Chronic pain severely affects Mrs HR’s day to day living; it reduces her general activity, mood and walking ability. She is unable to work normal hours as she is unable to concentrate when her pain is at its worst; as a result she has given up her social life to focus on her work. Her relationships with other people have suffered as a result of her chronic pain, so has her sleep and enjoyment of life. Section B Chronic pain is an abnormal somatosensory processing in the peripheral and central nervous system that persists longer than would normally be expected relative to the stimulus.1 The pain does not subside despite apparent healing of the initial injury and there is no known physiological purpose. Pain is a complex phenomenon that combines neurophysiological process with genetics, emotional state, attitudes, personality, circumstances and social context.2, 3 A major risk factor for the development of chronic neck pain is a previous episode of neck/black pain and/or persistent pain elsewhere in the body.4 HR has nociceptive/inflammatory somatic musculoskeletal chronic pain that is likely to be a result of her previous neck injuries. This section of the essay will focus on mechanisms of chronic pain development. It will outline peripheral and central pathophysiological changes that may have occurred in HR. Unfortunately however, it is not possible within the scope of this essay to detail the pathophysiological changes that can take place in the brain and the neuromatrix theory of pain.5 This essay will not discuss neuropathic pain. The disease process in chronic pain involves changes in the structure and function of the nervous system, as it is shaped and reshaped by the activity within. The nervous system has great plasticity. The CNS inhibits or amplifies the signals that the brain ultimately interprets as pain.6 HR’s chronic pain experiences include spontaneous pain, primary hyperalgesia (increased pain at the site of injury), secondary hyperalgesia (increased pain near the site of injury), and allodynia (pain caused by an innocuous stimuli). Activation, modulation and modification are different forms of plasticity that can result in pain hypersensitivity.6 Activation-dependant plasticity is where activation of nociceptive pathways manifests as a progressive increase in response of the system, to repeated stimuli. This can occur in nociceptive terminals in the periphery (autosensitisation) and in dorsal horn neurons (windup). Both these processes occur in normal physiological pain and usually reside after tissue repair, as they are normally activity dependant and reversible. Autosensitisation and windup can be contributing factors in the development of peripheral and central sensitisation.6, 7 Autosensitisation occurs when high threshold peripheral nociceptors become sensitive to lower threshold stimuli, this is due to changes in the transducers. The change in threshold of nociceptive neurons can also be due to an increase in the excitability of the peripheral nociceptive membrane terminal, this is termed heterosensitisation.6 Windup occurs when repetitive low-frequency activation of nociceptors (C-fibres) in the periphery by noxious stimulus cause fast EPSP (excitatory post-synaptic potential) in the dorsal horn.8 This results in co-release of neuromodulators and glutamate that produce slow EPSPs from wide dynamic range neurons. This results in temporal summation of nociceptive inputs and increased responsiveness of the neurons. Increased responsiveness also occurs when NMDA receptor currents, caused by peripheral inflammation removes the Mg2 block at NMDA receptors. This increased receptor activation further stimulates Ca2 channels and causes an increase in Ca2 influx and intracellular Ca2 release. This results in an increased action potential discharge from the neuron, which is known as windup.6, 9 Modulation of peripheral terminals is due to sensitising agents acting on receptors causing an inflammatory response. Central sensitisation is triggered by repetitive input from peripheral nociceptors which causes an increase in excitability of dorsal horn neurons. This causes an enhanced intensity of pain that outlasts the initial input. This process may require a low-level of pathology or inflammation in the periphery. Modulation can be due to numerous mechanisms and is potentially reversible. Mechanisms of modulation include phosphorylation of ion channels, receptors or regulatory peptides. This can change the intrinsic functional properties of expressed channels in the cell surface of primary sensory and dorsal horn neurons. Innocuous stimuli can cause an amplified response in the pain pathways in central sensitisation. This is linked to NMDA receptor activity and can involve AMPA receptors. Central sensitisation is associated with the depression of spinal inhibitory mechanisms, through the activation of NMDA receptors.6, 10, 11 Activation of the NMDA receptors by glutamate in the dorsal horn can contribute to central sensitisation, a mechanism that underpins the process of pain hypersensitivity (hyperalgesia and allodynia in the case of HR) in chronic pain. AMPA receptors are connected physically to NMDA receptors (NMDAR) in the dorsal horn. Normally Mg2 inhibits NMDAR activity and intracellular kinases are not active. Inflammation in the periphery causes the removal of Mg2 and NMDA activation. This causes a Ca2 influx through NMDAR which activates intracellular Ca2 dependant kinases PKC (protein kinase C), PKA (protein kinase A) and CaMKII (Ca2 /calmodulin-dependant protein kinase II). These activated kinases phosphorylate the GluR1 and cause the events leading to its insertion into the membrane. The activated PKC phosphorylates GluR2 at Ser880, therefore disrupting the binding of GluR2 to ABP(AMPAR-binding proteins)/GRIP(glutamate receptor-interacting protein), causing the internalisation of GluR2. These processes cause AMPARs to switch from being Ca2 impermeable (GluR2 containing AMPAs) to Ca2 permeable (GluR2 lacking AMPAs). This causes a further Ca2 influx and activation of Ca2 dependant kinases PKC, PKA and CaMKII. This positive feedback loop may be one of the pathways of central sensitisation in inflammation induced chronic pain.7, 12 Disinhibition of descending inhibitory neurons can also occur, causing pain to be increased. Activation of A-delta primary sensory neurons can cause depression of GABA/Glycine releasing inhibitory neurons. The depression requires NMDA receptor activation and post-synaptic Ca2 increase.13 Modification represents long-lasting changes that alter and distort the normal stimulus-response properties of the pain system. The changes can affect gene expression in ion channels, receptors and transmitters and it can alter connectivity, structure and the survival of neurons.6 The features of central sensitisation in neurons include the change of nociceptive specific neurons to wide dynamic range neurons that respond to noxious and innocuous stimuli, a progressive increase in responses caused by repeated innocuous stimuli (windup), expansion of the spatial input, and changes that outlast the initial trigger. This can result in spontaneous discharge, an increased receptive field (possible mechanism of secondary hyperalgesia), and an increased responsiveness to innocuous stimulus in the peripheral receptive field (a possible cause of allodynia).4 A-beta fibres can become sensitised in response to a noxious stimuli. This can result in A-beta fibres producing substance-P and causing the perception of pain, this is a characteristic of central sensitisation. 14, 15 Neuropeptides such as substance-p can diffuse away from its site of release in the dorsal horn and are not inactivated completely by reuptake mechanisms, therefore they are able to excite surrounding excitable neurons/membranes.7 This could result in the increased excitability and the unlocalised nature of Mrs HR’s chronic pain. Genetic alterations that affect the genes involved in sodium channels may cause the perception of pain, even without a noxious stimulus.2 Glial cells in the CNS can respond to painful stimuli by releasing cytokines. These cytokines have the ability to sensitise post-synaptic receptors and increase the release of neurotransmitters from pre-synaptic neurons.16, 17 Microglia and astrocytes can influence neuronal hypersensitivity when activated from their usual quiescent state by injury or inflammation in the CNS. These cells are thought to reduce inhibition, causing an increased pain perception.7 Section C Chronic pain is often not well controlled despite the use of analgesics. It is important to use psychological therapies and other techniques such as CBT and relaxation, as a multidisciplinary approach is essential. The focus of treatment for Mrs HR is to reduce her symptoms and pain to a manageable level that is balanced with the negative side effects of her medication. The treatment of chronic pain should be addressed using the biopsychosocial model of pain. This section of the essay will explain the mechanisms of action of dihydrocodeinine tartrate, its interactions, side effects that are relevant to the patient. HR had co-codamol changed to modified release DHC as she was experiencing disturbed sleep when her co-codamol wore off at night. HR also experienced constipation whilst taking co-codamol. This is a common side effect of opioids due to their action on μ and κ opioid receptors on neuronal plexuses in the gut wall. DHC is a semi-synthetic opioid used for the treatment of chronic pain. DHC is classified as a WHO step two analgesic for managing moderate pain. It is also used as an anti-tussive and as a substitute drug in the treatment of heroin addiction. The side effects of DHC are reduced by using a modified release dosage form. DHC modified release can be used to maintain therapeutic optimal blood levels for extended time periods and reduce side effects, such as nausea, vomiting and constipation. A pack of 56 modified release DHC continus tablets (dihydrocodeine tartrate) at 60mg each costs £5.18. DHC has a half life of three to five hours and is eliminated by metabolism (see appendix A). DHC has a low oral bioavailability due to the fact that it undergoes extensive first pass metabolism. The chemical or metabolites that contribute to the analgesic effect of DHC are unknown. There are no cautions for DHC use with the patient. There are no significant interactions for the patient taking DHC. Morphine can increase the bioavailability of gabapentin, but this has not been proven in DHC. Alcohol and opioids taken together can cause alcohol-enhanced hypotensive and sedative effects. Long-term use of opioid analgesics can lead to hyperalgesia. Treatment of opioid induced hyperalgesia include, reducing the dose of opioid or switching therapy and referring to a pain specialist clinic. Opiods can cause downsiness and may affect the performance of skilled tasks. This could seriously affect the patient as she wouldn’t be able to drive to work. Opiod recptors are coupled to inhibitory G-proteins. Opioid receptor activation inhibits adenylate cyclase and the production of intracellular cAMP. The G-proteins are directly coupled to K channels. The binding of opioids to opioid receptors increases K conductance. This hyperpolarises the cell, making it more difficult to depolarise. The reduced ability of the cell to depolarise inhibits neuronal voltage-gated Ca2 channels and reduces neurotransmitter release. μ-receptor stimulation in the raphe magnus of the brain reduces activity in the GABA (gamma-aminobutyric acid) neurons that project to serotonergic neurons in the brainstem. This causes increased firing of descending inhibitory serotonergic neurons that connect pre-synaptically with sensory nociceptive fibres in the dorsal horn of the spinal cord. This inhibits the release of pain causing metabolites, such as substance p, glutamate and nitric oxide from nociceptive neurons. Peripheral nerves contain μ -recptors and activation of these by an opioid angonist reduces the sensitivity to painful stimuli, especially in inflammatory pain. DHC can cause dependency and is subject to abuse, but it is rare as DHC does not give the euphoria that other opioids do. It is vital that opioid treatment is never abruptly withdrawn after long-term treatment, due to dependency and withdrawal side effects. Section D Psychological and social factors can be contributory in the development of chronic pain and in turn they can be caused by chronic pain. Approximately 12% of the general population suffer from chronic pain and an estimated 119 million working days were lost in 2007 due to back pain alone. It can have a detrimental effect on physical and psychological health, daily life, employment, and finances of the person affected. Chronic pain can have a negative impact on friendships and family life and it can be a considerable burden to the healthcare system and the economy. Chronic pain has a major impact on the wider economy; the total cost of back pain alone was £12.3 billion in 2000. HR risks losing her job, as she is finds it difficult to cope with her pain at work. This is causing her a great deal of emotional distress and results in her sacrificing her hobbies and social time to focus on her work. Work related factors can increase acute and chronic musculoskeletal pain, especially in females. Patients with chronic pain may have perceptions and beliefs about their work which can act as an obstacle to their recovery. Although HR has a stressful job, she finds that it gives her a purpose, as her goals in life are career focused. Working causes HR’s pain to increase and results in her being unable able to relax and enjoy a social life. This is likely to cause increased stress and its negative consequences. Physical stress and tension from prolonged computer work can prolong chronic pain. The distress exacerbates or complicates the pain, preventing natural healing. Patients experiencing chronic pain are more likely to have psychopathology that the general population. Pain can promote depression and likewise depression can promote pain. The number of cases where depression is accompanied by pain is between 15-100%???????. Depression and intensity of pain are significant risk factors in the development of chronic pain. Females are more likely to have pain and depression and have a low response to treatment. HR’s chronic pain and its associated symptoms could have a negative effect on her relationship with her husband and friends. Excess negative thinking or catastrophising about pain and the fear of movement or reinjury are important factors in the development of chronic pain and its associated disability. HR has little control over her pain. Patients who have control of their pain and associated symptoms are better able to cope with chronic pain and resulting disability than those who are passive to a threat or believe they do not have control. Distraction from pain can be beneficial for the patient as they focus less on the pain experience therefore less pain is perceived. Being able to predict the effects of pain with relative certainty can help a patient deal with their chronic pain. It is vital for the patient to know the aetiology of their pain so that they are less worried and concerned, as this allows the patient to cope better. Avoidance of activities and fear of causing further pain can be detrimental in chronic pain, whilst in acute pain they are vital for recovery. The patient may become anxious, therefore reducing her pain threshold and tolerance, causing pain to increase in intensity. A belief that activity may worsen the initial injury can result in avoidance of activities. This can stop rehabilitation and lead to physical de-conditioning, causing further pain and disability. This is a self-stoking cycle. The fear of pain can be more disabling than pain itself in some patients. Patients with neck pain may have a changed pattern of motor control, whereby they use their painful muscles less and use their accessory neck muscles more. Thus causing physical de-conditioning of their postural cervical region muscles and increasing the pain experienced. Cognitive coping strategies can affect a person’s perception and tolerance of pain sensitisations. The avoidance-endurance model of chronicity of pain can be applied to Mrs HR. After her injuries causing acute pain the patient may have minimised her thoughts about the pain and maintained a positive mood, thus having a suppressive behaviour. Mrs HR may have overdone movements, exercise and her work which caused muscular hyperactivity. Overtime this may have contributed significantly to her chronic pain and its increasing intensity. Conclusion The pain system has multiple pathways, with numerous synaptic junctions, complex networks of local and remote controls acting at each junction all with a capacity for neuroplastic change. Pharmacological treatments alone do not always suffice in the management of such a mutli-factorial condition and therefore treatment requires a truly holistic multidisciplinary approach to treat not only the pain but the psychological, social and economic issues of chronic pain. 1. Rashiq ES, P. Taenzer, P. Jonsson, E. In: Chronic Pain: a Health Policy Perspective. Health Care and Disease Management. 2008:59-66. 2. Devulder JE. The puzzle of chronic pain: will genetics force a major breakthrough in the pathophysiology and the treatment of chronic pain? Acta Clin Belg. 2006 Jan-Feb;61(1):1-4. 3. Serpell M. Anatomy, physiology and pharmacology of pain. SURGERY 24:10: Elservier; 2006. 4. Sterner Y, Gerdle B. Acute and chronic whiplash disorders–a review. J Rehabil Med. 2004 Sep;36(5):193-209; quiz 10. 5. Melzack R. Pain and the neuromatrix in the brain. J Dent Educ. 2001 Dec;65(12):1378-82. 6. Woolf CJ, Salter MW. Neuronal plasticity: increasing the gain in pain. Science. 2000 Jun 9;288(5472):1765-9. 7. Latremoliere A, Woolf CJ. Central sensitization: a generator of pain hypersensitivity by central neural plasticity. J Pain. 2009 Sep;10(9):895-926. 8. Elliott JM, Noteboom JT, Flynn TW, Sterling M. Characterization of acute and chronic whiplash-associated disorders. J Orthop Sports Phys Ther. 2009 May;39(5):312-23. 9. Teasell RW. Pathophysiology of chronic pain disorders. Clin J Pain. 2001 Dec;17(4 Suppl):S8-9. 10. Meyr AJ, Saffran B. The pathophysiology of the chronic pain cycle. Clin Podiatr Med Surg. 2008 Jul;25(3):327-46; v. 11. Schaible HG, Schmelz M, Tegeder I. Pathophysiology and treatment of pain in joint disease. Adv Drug Deliv Rev. 2006 May 20;58(2):323-42. 12. Tao YX. Dorsal horn alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor trafficking in inflammatory pain. Anesthesiology. 2010 May;112(5):1259-65. 13. Jensen TS. Pathophysiology of pain: from theory to clinical evidence. European Journal of Pain. 2008;2:13-7. 14. Woolf CJ, Doubell TP. The pathophysiology of chronic pain–increased sensitivity to low threshold A beta-fibre inputs. Curr Opin Neurobiol. 1994 Aug;4(4):525-34. 15. Greene SA. Chronic pain: pathophysiology and treatment implications. Top Companion Anim Med. 2010 Feb;25(1):5-9. 16. Woolf CJ, Decosterd I. Implications of recent advances in the understanding of pain pathophysiology for the assessment of pain in patients. Pain. 1999 Aug;Suppl 6:S141-7. 17. Scholz J, Woolf CJ. The neuropathic pain triad: neurons, immune cells and glia. Nat Neurosci. 2007 Nov;10(11):1361-8.
Review the Institute of Medicine’s 2010 report “The Future of Nursing: Leading Change, Advancing Health.” 750‐1,000 words, discussing the influence of the IOM report on nursing practice. Include the
order essay cheap ” 750‐1,000 words, discussing the influence of the IOM report on nursing practice. Include the following: Summarize the four messages outlined in the IOM report and explain why these are significant to nursing practice. Discuss the direct influence the IOM report has on nursing education and nursing leadership. Describe the benefits and opportunities for BSN‐prepared nurses. Explain why it is important that a nurse’s role and education evolve to meet the needs of an aging and increasingly diverse population. Discuss the significance of professional development, or lifelong learning, and its relevance in caring for diverse populations across the life span and within the health‐illness continuum. Discuss how nurses can assist in effectively managing patient care within an evolving health care system. Prepare this assignment according to the guidelines found in the APA Style Guide. An abstract is not required.
The Importance of Education during Early Childhood Qualitative Research Essay
The Importance of Education during Early Childhood Qualitative Research Essay. Introduction In pre-school children life, parents play an integral role in influencing children’s learning experiences and knowledge grasps. This arises from interactive segments among parents and children. For this reason, many parents opt to participate in mothers and toddlers groups, childcare arrangements, babysitting activities, and other events that increase interactive sessions between toddlers and parents. Such programs harbor potential positive impacts child development through provision of high quality, individualized, social reactions, and catalyzing experiences that improves children learning capabilities. Conversely, poor parenting, inadequate interactive parent-children structures, and minimal supervision of toddlers negatively affect development of children. Such negativities hold deleterious bearing on children’s abilities to grasp information, leading to lackluster performance in class work. Definition of key words Child development refers to the physical, social, intellectual, and emotional growth in young people as they interact with peers, parents, teachers, and the society. Development in children makes them more independent of parental guidance. Knowledge passage, on the other hand, denotes the transfer of familiarity and mastery of concepts about something in the society. It takes place in children through peer competition, parental education, and teachers’ guidance. Pre-school years represent stages in life when children start developing before achieving the school going age. Most scholars put ages 1 to 4 years as the pre-school years (Sheridan, Sharma,The Importance of Education during Early Childhood Qualitative Research Essay
A Critique of an Academic Journal by Luis Garay and Xavier Font Essay (Critical Writing)
Introduction This paper provides a critical analysis of the article: “Doing good to do well? Corporate social responsibility reasons, practices and impacts in small and medium accommodation enterprises”. The article is authored by Luis Garay and Xavier Font. The author’s arguments are based on a comparison of corporate social responsibility with corporate financial performance. The topic is lengthy and broad. Therefore, the author has not specified the role of small and medium enterprises in sustainable hospitality management. The article begins with a review of corporate responsibility and corporate financial performance. This article further presents the analyses of the relationship between corporate social responsibility and corporate financial performance1. A critical evaluation of the author’s argument(s), assumptions made by the author, and the main implications The main argument of the author is that corporate social responsibility and corporate financial performance affect hospitality management. The greatest challenge to the argument is that misguided assumptions are made, which can be misleading to the reader. The article places corporate social responsibility at a static position instead of appreciating the influential dynamism towards hospitality. The author has discussed the topic by exploring several assumptions about the hospitality environment instead of presenting evidence-based research concerning the topic2. The authors review the literature about corporate financial responsibility and corporate social responsibility. The literature review is analyzed before the authors provide an introduction to the meaning of corporate social responsibility and corporate financial responsibility. There is a need to provide in-depth analyses of how the two sectors are likely to be affected by a large percentage of recorded accommodation rates3. From the outset, the reader is caught at a crossroad whereby he/she cannot understand the goals of the authors. The goals tend to be hidden from the reader and the reader must search the goals of the article because they are scattered. The authors present an analytical evidence-based analyses but this has been done at a broad scope. Similarly, the authors present the main theories for the tourism sector to engage in corporate social sustainable and corporate financial performance. Get your 100% original paper on any topic done in as little as 3 hours Learn More The article presents the methodology, and it is evident that qualitative research has been applied. The authors ought to have considered using the qualitative and quantitative methods of research to present reliable results4. The purpose of the article is to show how the constant change and the dynamic nature of corporate social responsibility and corporate financial performance have affected the accommodation and the tourism sector. However, the authors have emphasized on applying the wrong approach in achieving the purpose of the article. The authors have adopted a fixed approach instead of using the principles approach. The validity of the different scenarios that have been applied using the fixed approach cannot be fully relied upon to achieve the end purpose. The fixed approach method is grounded on the gradual approach of responsibility of various institutions. However, this has been done with the outlook on the main role and the influences on the key stakeholders in the industry. The fixed approach has various weaknesses because it does not prioritize the actions and the direct consequences of corporate responsibility and its role in the tourism sector. The data gathered through this approach is tainted with positive, negative and neutral results5. A critical evaluation of the accuracy and relevance of evidence that is utilized in the article The article relies on secondary evidence. The evidence is gathered through the qualitative research method. The article has supported the topic with academic data but the method used leaves a lot to be desired. The authors should have combined the qualitative and quantitative research methods. It is well known that a well researched article is based on varied information6. Articles aimed at researching the relationship of two strong variables, the evidence in the research should be reliable. The evidence in the article presents good management approach, whereby the authors argue that the corporate social responsibility and corporate financial performance produce reliable results if they are well managed. The article seeks to answer the question why and how the relationship between the corporate sustainable responsibility and corporate finance performance affect small and medium accommodation enterprises. The authors should have used the principles approach because it focuses on the impacts of the relationship between the above mentioned factors and how the impacts affect the tourism industry7. We will write a custom Critical Writing on A Critique of an Academic Journal by Luis Garay and Xavier Font specifically for you! Get your first paper with 15% OFF Learn More The authors have used the stakeholder approach, whereby they presented the impact of the interaction of the tourism industry on the corporate sustainable responsibility and how the relationship stretches from economic level to legal level. The stakeholder interaction and the capabilities presented are innovation and higher integration, which has assisted in transforming the tourism and management industry. The article presents the main objective to show how business engagement assists in achieving competitive advantage. The main weakness of the article is realized by the failure to mention other factors which enhance competitiveness as far as sustainable practices is hospitality and tourism management is concerned. The article fails to bring the desired link between competitive advantages and its application in the tourism business8. The presentation of the evidence to support the authors’ arguments is well cited but limited. The author appreciates the scarcity of the literature that relate to the topic of tourism corporate social responsibility. The literature available, which has been reviewed on the contribution of corporate responsibility in explaining the tourism behavior, takes a broad stand. The narrowing down of the arguments provides doubtful literature, which cannot be relied on. The literature presented provides the reader a chance to doubt because a reliable article is based on stable evidence which can persuade9.On the other hand, the corporate sustainable responsibility literature is limited to the environmental practices which have positive impacts on tourism management10. A critical evaluation of clarity, rigor, and other aspects of the article The article has achieved the underlying principles surrounding clarity. The article is not only unclear but it also carries broad overview of main aspects under investigation. The convincing power of the article is mainly eroded with main assurances on the capacity to cover the topic, and this causes the article to be elusive. The fact that the corporate social responsibility and corporate financial performance are overlapping in the discussion, makes it hard to identify the relationship with small and medium accommodative purposes. The article states the importance of responsibility practices but additional information to show how and why is a major weakness of the article is lacking.11 Conclusion The article presents the salient arguments and the assumptions in identifying the importance of corporate social responsibility and corporate finance management in the tourism industry. The implications of the assumptions in the article have been evaluated. Not sure if you can write a paper on A Critique of an Academic Journal by Luis Garay and Xavier Font by yourself? We can help you for only $16.05 $11/page Learn More The critical evaluation of the evidence used is also considered. The assessment of how clear and convincing the article is has been discussed. The conclusion is to the effect that the main objective of the article is not reached due to the use of broad topic and lack of narrowing down to a specific aspect. Bibliography Garaya, L,
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