Idiopathic Pulmonary Fibrosis: An Overview

Idiopathic Pulmonary Fibrosis: An Overview Jennifer Beardsley Abstract Idiopathic pulmonary fibrosis (IPF) is a devastating interstitial lung disease that has no cure. The term fibrosis refers to scarring, in IPF particularly the scarring of the lungs. The scarring causes irreversible destruction and progressive decline of the lungs. When the tissue thickens, the lungs cannot properly exchange oxygen. The term idiopathic, in medicine, means that the origin of the disease is unknown. The exact cause of IPF is unknown, however, certain risk factors such as smoking, exposure to inhaled toxins such as asbestos, lung injury, viral, and bacterial infections, acid reflux and genetics associated with the disease. IPF mainly affects people ages 50 and up. â€Å"Many people live only about 3 to 5 years after diagnosis. The most common cause of death related to IPF is respiratory failure† (â€Å"What Is Idiopathic Pulmonary Fibrosis? NHLBI, NIH,† n.d.). â€Å"40,000 people die each year to IPF, the same as to breast cancer† (â€Å"Facts Abou t Idiopathic Pulmonary Fibrosis | Coalition For Pulmonary FibrosisCoalition For Pulmonary Fibrosis,† n.d.), yet IPF is still an unknown disease to many people. This paper will discuss the risk factors, disease process, complications, management, and new drug therapy clinical trials. Idiopathic Pulmonary Fibrosis: An Overview Etiology Idiopathic Pulmonary Fibrosis first started to become recognizable around the late 1800’s (Noble Homer, 2005). While currently the exact cause is unknown, there have been several risk factors that are recognized to contribute to the disease. As mentioned above, smoking, exposure to inhaled toxins such as asbestos, lung injury, viral and bacterial infections, acid reflux and genetics are associated with the disease (Noble Homer, 2005). Smoking accelerates the loss of lung function by destroying the cilia inhibiting the lungs natural ability to clean and repair itself (Oh, Murray, Molfino, 2012). Smoking also damages alveoli, causing poor gas exchange. The chemicals in cigarettes contribute to lung decline and disease and coat the lungs with tar and toxins (Oh et al., 2012). Inhaled substance and toxins such as asbestos are hypothesized to increase IPF probability (Meltzer Noble, 2008). When toxins invade the lungs, they interfere with the alveoli gas exchange process (Meltzer Noble, 2008). Lung injury can cause permanent damage. Acute lung injury has been hypothesized to accelerate an underlying progression of IPF. When cells of the lungs are damaged, it can be irreversible (Kottmann, Hogan, Phipps, Sime, 2009). Viral and bacterial infections cause a build of mucus in the lungs. When the alveoli get clogged they cannot properly exchange oxygen and carbon dioxide. Each infection acquired can cause more damage and can lead to permanent damage. When the lungs lose their ability to exchange gas, oxygen is inhibited from reaching the body’s vital organs (Kottmann et al., 2009). GER, commonly known as acid reflux, occurs when acid is aspired into the esophagus. â€Å"Researchers have found that 9 out of 10 people who have IPF also have gastroesophageal reflux disease† (â€Å"What Causes Idiopathic Pulmonary Fibrosis? NHLBI, NIH,† n.d.) Recent research has found that genetics may play an important role in the risk factor of developing IPF. â€Å"Over the past decade, one aspect that has held great promise in helping the medical community to better define the pathogenesis of IPF is the recognition that genetic factors may play a role in this disease† (Lawson, Loyd, Degryse, 2011). Pathophysiology The cause of IPF is unknown. Despite considerable advancement in understanding the progression of IPF, the knowledge of the beginning stages of IPF re still inadequately understood (Noble Homer, 2005). Originally, in the 1970’s, it was thought that inflammation of the alveoli was the cause (Noble Homer, 2005). It was believed that untreated inflammation leads to the scarring of the lungs. Anti-inflammatory and corticosteroids were widely used to treat the inflammation. However, those therapies have proven ineffective, making it evident that inflammation was not the cause (Dempsey, Kerr, Gomersall, Remmen, Currie, 2006). The second theory that came about in the 1980’s suggesting growth termed â€Å"alveolar macrophage-derived growth factor† (Noble Homer, 2005). Known as the ‘growth factor hypothesis’, it is believed that abnormal healing of trauma within the lungs exaggerates the response and growth of profibrogenic causing the scarring of IPF (Noble Homer, 2005). This theory still proves to be a highly important discovery in the pathophysiology of IPF (Dempsey et al., 2006). A third theory also came out of the 1980’s, known as the epithelial-mesenchymal hypothesis, suggests that tissue death of alveolar epithelial cells can lead to alveolar collapse (Noble Homer, 2005). The epithelial- mesenchymal cell conversion can alter and change motility and the ability to heal. â€Å"Imbalance of the normal homeostatic microenvironment might be, per se, a cause of fibroblast proliferation and myofibroblast differentiation leading to fibrosis† (Prunotto et al., 2012). Clinical Manifestation According to the Coalition for Pulmonary Fibrosis, â€Å"Idiopathic pulmonary fibrosis (IPF) is a progressive and generally fatal disease characterized by scarring of the lungs that thickens the lining of the lungs, causing an irreversible loss of the tissue’s ability to transport oxygen. IPF ultimately robs a patient of the ability to breathe†(â€Å"Facts About Idiopathic Pulmonary Fibrosis | Coalition For Pulmonary Fibrosis,† n.d.). IPF usually occurs in older adults in their 50’s or 60’s, and tends to occur more in men than in women (Lawson, Loyd, Degryse, 2011). According to the Coalition For Pulmonary Fibrosis, IPF affects about 128,100 people in the United States, with 48,000 new cases diagnosed annually (â€Å"Facts About Idiopathic Pulmonary Fibrosis | Coalition For Pulmonary Fibrosis,† n.d.). â€Å"IPF has been reported to occur throughout the world in many different racial and ethnic groups. Studies in the United States have sugge sted that Caucasians are more likely to be diagnosed with IPF and have higher mortality rates from IPF than African Americans. It is unclear if these findings are due to real differences in racial characteristics or to an under-diagnosis of this condition in minority populations† (Siegel, 2011). IPF symptoms develop over time and usually are not diagnosed until serious damage has already been done to the lungs (â€Å"What Are the Signs and Symptoms of Idiopathic Pulmonary Fibrosis? NHLBI, NIH,† n.d.). Patients are often misdiagnosed with diseases that present similar symptoms such as Chronic Obstructive Pulmonary Disorder (â€Å"Facts About Idiopathic Pulmonary Fibrosis | Coalition For Pulmonary Fibrosis,† n.d.). Idiopathic pulmonary fibrosis usually present gradually with a nonproductive cough and dyspnea. (Hyzy, Huang, Myers, Flaherty, Martinez, 2007). The main symptom patients complain of being shortness of breath (Noble Homer, 2005). Other common symptoms include: â€Å"dry, hacking cough; rapid, shallow breathing; gradual, unintended weight loss; Fatigue (tiredness) or malaise (a general feeling of being unwell); clubbing, which is the widening and rounding of the tips of the fingers and toes† (â€Å"What Are the Signs and Symptoms of Idiopathic Pulmonary Fibrosis? NHLBI, NIH,† n.d.). The gold standard for diagnosis of patients with IPF is a surgical lung biopsy (SLB), however critical risk for these patients usually prevent a high-risk surgical procedure (Kaarteenaho, 2013). â€Å"The mortality, which can occur shortly after the procedure, has probably been the major reason to refrain from performing SLB† (Kaarteenaho, 2013). With that in mind, diagnosis of IPF includes clinical, radiologic and histopathologic aspects (Wolters, Collard, Jones, 2014). The American Thoracic Society states, â€Å"in the absence of a definitive lung biopsy, the presence of all four major criteria and three minor criteria, as set forth in the current guidelines, increases the likelihood of a correct diagnosis of IPF: Major Criteria †¢Exclusion of other known causes of interstitial lung diseases, such as certain drug toxicities, environmental exposures, and connective tissue diseases †¢Abnormal pulmonary function studies that include evidence of restriction (reduced vital capacity often with an increased FEV:FVC ratio) and impaired gas exchange (increased AaPO2 with rest or exercise or decreased DLCO) †¢HRCT scan showing bibasilar reticular abnormalities with minimal ground-glass opacities †¢Transbronchial lung biopsy or BAL showing no features to support another diagnosis Minor Criteria †¢Age >50 years †¢Insidious onset of otherwise unexplained dyspnea on exertion †¢Duration of illness greater than or equal to 3 months †¢Bibasilar inspiratory crackles (dry or â€Å"Velcro-like† in quality)† (Raghu et al., 2011). The physical assessment is an important part of diagnosis, however, symptoms can mimic other diseases and make it hard to differentiate (Meltzer Noble, 2008). Attention should be paid to key risk factors such as work related inhaled chemical exposure and smoking. Fine inspiratory â€Å"Velcro-like† crackles can be heard upon examination and advance towards the upper airway as the disease progresses (Meltzer Noble, 2008).Clubbing of the fingers and toes is found in 50% of patients (Meltzer Noble, 2008). Lab results are often inconclusive to IPF, but as part of a puzzle can help to identify the disease. An ABG will more than likely read normal (Meltzer Noble, 2008). The pulmonary function test (PFT) can lend valuable information to diagnosing IPF. While IPF is a restrictive disease, it can often imitate obstructive disorders or congestive heart failure (CHF) (Meltzer Noble, 2008). â€Å"Routine spirometry reveals decreased measures of forced vital capacity (FVC) and forced expiratory volume in one second (FEV1). The ratio of FEV1/FVC remains normal (or increased) in IPF, consistent with restrictive physiology† (Meltzer Noble, 2008). Subsequently, the PFT can also reveal reduced TLC, RC, and RV. Reduced gas transfer may also be noted with a DLCO (Meltzer Noble, 2008). Almost every patient with Idiopathic Pulmonary Fibrosis will have abnormal radiological findings (Meltzer Noble, 2008). The imaging modality of choice in diagnosing IPF is High-resolution computed tomography (HRCT) (Hospenthal, 2006). â€Å"Patchy, predominantly peripheral, subpleural, bibasal reticular opacities, often associated with traction bronchiectasis† (Harari Caminati, 2005). A phenomenon referred to as honeycombing is a prevalent finding in IPF, seen below is figure 3. Figure 1: Chest radiograph of a patient with IPF. Chest radiograph reveals peripheral, subpleural reticular opacities, most profuse at the lung bases (Harari Caminati, 2005). Figure 2: Chest HRCT in a patient with IPF. HRCT shows patchy, predominantly peripheral, subpleural, bibasal reticular abnormalities, traction bronchiectasis and bronchiolectasis and irregular septal thickening. There is also ground glass (Harari Caminati, 2005). Figure 3: Chest HRCT in a patient with IPF. HRCT shows predominantly peripheral and subpleural fibrosis with honeycombing (Harari Caminati, 2005). Complications Idiopathic pulmonary fibrosis is a highly progressive disease. Because the tissues in the lungs are scarred, they cannot properly exchange gas and the low amount of oxygen delivered to the body causes several complications and puts strain on the right side of the heart. According to the America Thoracic Society, â€Å"There is an increasing awareness of complications and comorbid conditions frequently associated with IPF† (Raghu et al., 2011). Some of the most common complications are: Pulmonary hypertension, cor pulmonale, respiratory failure and lung cancer (Daniels, Yi, Ryu, 2008). Depression is also often seen in people with IPF because of its devastating prognosis (â€Å"Living With Idiopathic Pulmonary Fibrosis NHLBI, NIH,† n.d.). Acute exacerbations (unexplained worsening of dyspnea) of IPF represent the most destructive and deadly complication (Raghu et al., 2011). â€Å"It is presently unclear if acute exacerbation of IPF is simply a manifestation of an unid entified respiratory complication (such as pulmonary emboli, infection) contributing to an acute worsening in a patient with IPF or represents an inherent acceleration in the pathobiological processes involved in IPF† (Raghu et al., 2011). Medical Management There is currently not a cure for idiopathic pulmonary fibrosis (â€Å"What Is Idiopathic Pulmonary Fibrosis? NHLBI, NIH,† n.d.). Until recently, primary methods of management have been anti-inflammatories and lung transplants (Dempsey, Kerr, Gomersall, Remmen, Currie, 2006). While Anti-inflammatory are still used today it is not due to the effectiveness of treatment, but lack thereof for alternatives (Dempsey et al., 2006).â€Å"Immunosuppressive or cytotoxic agents are used among steroid nonresponders, patients experiencing serious adverse effects from corticosteroids, and patients at high risk for corticosteroid complications† (Harari Caminati, 2005). â€Å"Single-lung transplantation results in an actuarial survival of 73% at 1 year and 57% at 3 years† (Harari Caminati, 2005). Unfortunately, most patients are not eligible for transplant due to age or comorbidity factors (Harari Caminati, 2005). In the spring of 2014 the FDA announced two new drugs for the management of IPF (â€Å"CPF Celebrates Historic Year of Progress in Pulmonary Fibrosis | Coalition For Pulmonary Fibrosis Coalition For Pulmonary Fibrosis,† n.d.). Ofev (nintedanib) and Esbriet (pirfenidone) were both shown to slow the progress of IPF in clinical trials. â€Å"Pirfenidone is a transforming growth factor-beta inhibitor and tumor necrosis factor-alpha inhibitor† (Gohil, 2015). Ofev is a â€Å"fibroblast growth factor receptor (FGFR) antagonist, platelet-derived growth factor receptor (PDGFR) antagonist, and vascular endothelial growth factor receptor (VEGFR) antagonist† (Gohil, 2015). The two treatments are still in the early stages with little known about their effectiveness. Prognosis Prognosis for IPF is dim. It is a fatal disease (Meltzer Noble, 2008). The median survival rate is 3 years after diagnosis (Peljto et al., 2013). Factors associated with â€Å"shortened survival time include: older age, smoking history, lower body mass index (BMI), more severe physiologic impairment, greater radiologic extent of disease, and the development of other complications or conditions, in particular, pulmonary hypertension, emphysema, and bronchogenic cancer† (Ley, Collard, King, 2011). Clinical Trials During the past decade, there has been a notable amount of research into the treatment of idiopathic pulmonary fibrosis. IPF is no longer believed to be due to inflammation, but multiple injuries with atypical cell repair. According to The Coalition for Pulmonary Fibrosis, â€Å"there are many therapies under investigation in clinical trials that include: †¢Antifibrotic or antifibrogenic agents (such as Pirfenidone, interferon and certain blood-pressure-lowering medications) to suppress the scarring process †¢Antioxidants (such as N-acetylcysteine) to prevent damage to lung tissue †¢Monoclonal antibodies to inhibit â€Å"bad† cytokines (protein growth factors, such as TGF-beta, TNF-Alpha, or CTGF, that activate inflammation)† (â€Å"Active Clinical Trials and Investigational Research in IPF | Coalition For Pulmonary FibrosisCoalition For Pulmonary Fibrosis,† n.d.). References Active Clinical Trials and Investigational Research in IPF | Coalition For Pulmonary FibrosisCoalition For Pulmonary Fibrosis. (n.d.). Retrieved February 17, 2015, from http://www.coalitionforpf.org/active-clinical-trials-and-investigational-research-in-ipf/ Facts About Idiopathic Pulmonary Fibrosis | Coalition For Pulmonary FibrosisCoalition For Pulmonary Fibrosis. (n.d.). Retrieved February 17, 2015, from http://www.coalitionforpf.org/facts-about-idiopathic-pulmonary-fibrosis/ Hospenthal. (2006). Diagnosis and management of idiopathic pulmonary fibrosis: Implications for respiratory care. Respir Care, 51, 382–391. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/16563193 Hyzy, R., Huang, S., Myers, J., Flaherty, K., Martinez, F. (2007). Acute exacerbation of idiopathic pulmonary fibrosis. Chest, 132, 1652–1658. doi:10.1378/chest.07-0299 Kaarteenaho, R. (2013). The current position of surgical lung biopsy in the diagnosis of idiopathic pulmonary fibrosis. Respiratory Research, 14, 43. doi:10.1186/1465-9921-14-43 Lawson, W. E., Loyd, J. E., Degryse, A. L. (2011). Genetics in pulmonary fibrosisfamilial cases provide clues to the pathogenesis of idiopathic pulmonary fibrosis. The American Journal of the Medical Sciences, 341(6), 439–43. doi:10.1097/MAJ.0b013e31821a9d7a Ley, B., Collard, H. R., King, T. E. (2011). Clinical course and prediction of survival in idiopathic pulmonary fibrosis. American Journal of Respiratory and Critical Care Medicine, 183(3), 431–440. doi:10.1164/rccm.201006-0894CI Meltzer, E. B., Noble, P. W. (2008). Idiopathic pulmonary fibrosis. Orphanet Journal of Rare Diseases, 3, 8. doi:10.1186/1750-1172-3-8 Noble, P. W., Homer, R. J. (2005). Back to the future: Historical perspective on the pathogenesis of idiopathic pulmonary fibrosis. American Journal of Respiratory Cell and Molecular Biology, 33(8), 113–120. doi:10.1165/rcmb.F301 Peljto, A. L., Zhang, Y., Fingerlin, T. E., Ma, S.-F., Garcia, J. G. N., Richards, T. J., †¦ Schwartz, D. A. (2013). Association between the MUC5B promoter polymorphism and survival in patients with idiopathic pulmonary fibrosis. JAMA, 309(21), 2232–9. doi:10.1001/jama.2013.5827 Raghu, G., Collard, H. R., Egan, J. J., Martinez, F. J., Behr, J., Brown, K. K., †¦ Schà ¼nemann, H. J. (2011). An Official ATS/ERS/JRS/ALAT Statement: Idiopathic pulmonary fibrosis: Evidence-based guidelines for diagnosis and management. American Journal of Respiratory and Critical Care Medicine, 183, 788–824. doi:10.1164/rccm.2009-040GL Siegel, M. D. (2011). Breathing in America: Diseases, Prognosis, and Hope. Critical Care Medicine, 39, 1857. doi:10.1097/CCM.0b013e31821b1e92 What Are the Signs and Symptoms of Idiopathic Pulmonary Fibrosis? NHLBI, NIH. (n.d.). Retrieved February 17, 2015, from http://www.nhlbi.nih.gov/health/health-topics/topics/ipf/signs What Is Idiopathic Pulmonary Fibrosis? NHLBI, NIH. (n.d.). Retrieved February 14, 2015, from http://www.nhlbi.nih.gov/health/health-topics/topics/ipf Wolters, P. J., Collard, H. R., Jones, K. D. (2014). Pathogenesis of idiopathic pulmonary fibrosis. Annual Review of Pathology, 9, 157–79. doi:10.1146/annurev-pathol-012513-104706

Essay on Sin in Sophocles Oedipus the King and Ibsens Ghosts

The Impact of Sin in Sophocles' Oedipus the King and Ibsen's Ghosts      Ã‚  Ã‚   Sophocles' play Oedipus the King was written for a Greek audience as a religious right and lesson around two thousand years ago, while Ibsen's play Ghosts was written as a criticism of the Norwegian society during the 1890's. Although these plays were written for very different reasons and under different circumstances, the universal theme connecting them is mankind's liability to sin because the results affect a greater whole. One of the more specific themes of these plays is the negative effect that parents' sins have upon the generations to follow.    In Oedipus the King, Oedipus is born the son of Laius and Jocasta, the king and queen of Thebes. However, when they hear Apollo's prophecy (that Oedipus will kill his father and sleep with his mother) they decide to destroy Oedipus. Apollo's prophecy made Oedipus an unwanted child. In this case, the parents' transgression of the law was that they attempted to defy the gods by evading Apollo's prophecy. Later Jocasta states that "no skill in the world, nothing human, can penetrate the future" (Sophocles 201). Oedipus, as a later response to her statement says, "...all those prophecies I feared - Polybus packs them off to sleep with him in hell! They're nothing, worthless" (Sophocles 214). In this way, Oedipus and Jocasta quit believing in the prophecies altogether. In Ghosts, Regine is the result of an affair that Captain Alving had with the housemaid, Johanna. Since Regine is a child born out of wedlock, she is unwanted by Captain Alving because she is the result of his sin, and if a nyone were to discover her true origins it could destroy the respect that society has for him. She is also unwant... ...ther sins and results that happened after that would never have occurred. In short, do not let your pride blind you to the knowledge of those who are wiser than you. In Ghosts, Ibsen's message is that the Norwegian society was hypocritical and unmoral. This is shown through Oswald's suffering because he is simply a victim who is paying for what a hypocritical society permits - men's immorality. The overall idea behind this play is that hypocrites should not criticize others; as Manders criticizes Oswald the companions that he chose during his stay in Paris. However, they are both combined by the intricate link of sin and its effects on the whole.    Works Cited Ibsen, Henrik. Four Major Plays. Trans. James McFarlane and Jens Arup. New York: Oxford UP, 1998 Sophocles. The Three Theban Plays. Trans. Robert Fagles. New York: Penguin Classics, 1984

Leadership practices Essay

The same situation applies to Technical know-how, I generally understand the technical know-how of my Job and maybe not clear with Just a few policies and procedures because I haven’t had the chance to deal with them. The interpersonal competence need to be developed further as I have not developed anything in that area in the business sense and some of the skills have been acquired in social groups such as the church. The Social-emotional competence also scored quite high which is really a true reflection as I am a person who is really concerned about emotional and wellbeing of the people where work is involved. The anagerial and entrepreneurial competences had average scores which are actually true, maybe because I am not really in a managerial level at work and I do believe that more need to be developed in this area. The intellectual competence had the lowest percentage score of 40% and I also do believe that I need the chance to develop and show my intellectual skills. B. The Managerial competence scored 50% which is Just an average value. According to Daft (2008, p. 15) Management focuses on establishing detailed plans and schedules for achieving specific results. This has similar characteristics to quadrant C of the whole brain model. What is whole brain thinking) shows that a person who has quadrant B (green) dominance has the following characteristics: organised, sequential, planned and detailed. The managerial competence has similar characteristics with the quadrant B and these two score sheets gave similar results. They showed average competence as a manager and the need to improve in this area. The inter-personal competence gives an average percentage which also when compared to the whole brain, the quadrant C (Red) is also has moderate results. The whole brain quadrant A (blue) had the highest results which confirmed the Job competence and technical know-how. I am an engineer by professional and hence so mathematical by nature of my Job. C. The ways of improving leadership effectiveness include From the Managerial competence, the percentage was 50% which implies there is more to be done in the area hence need to improve as a leader by learning to be a leader who should move from stability to change and Crisis Management (Daft 2008, p. 8). The whole competence analysis had varying percentages, Leadership effectiveness can be improved by becoming a learning leader thus â€Å"a leader who is open to learning and change and encourages the growth and development of thers† (Daft 2008, p. 2). Need to improve on intellectual competences by getting the big picture, a leader who is up to date with what is happening in the core area of business.

The Mind and Motivation of a Serial Killer Essay - 772 Words

The mind and motivation of a serial killer nbsp;nbsp;nbsp;nbsp;nbsp;Serial killers tend to be white heterosexual males in their twenties and thirties, who are sexually dysfunctional and have low self-esteem. Serial killers generally murder strangers with cooling off periods in between each murder. Serial killers are twisted in nature. Some return to the place the murder happened or the gravesite to fantasize about their deeds. Serial killers have made many excuses for their killings and behavior such as: Henry Lucas blamed his upbringing, Jeffrey Dahmer claims he was born with a à ¢Ã¢â€š ¬Ã…“partà ¢Ã¢â€š ¬? of him missing, Ted Bundy said porno made him do it and John Wayne Gacy turned the blame around and said the victims deserved to die. Many†¦show more content†¦Serial killers are sick people and their numbers seem to be growing. nbsp;nbsp;nbsp;nbsp;nbsp;Serial killers choose victims weaker than themselves. Many times their victims will fit a certain stereotype, which has symbolism for the killer. Ted Bundy killed college age girls with long brown hair. I wonder if he was killing over and over again the girl who broke his heart? Many serial killers will keep quot;souvenirsquot; of their crime, which later refuels the fantasy. When Bundy was asked why he took Polaroids of his victims, he said, quot;When you work hard to do something right, you dont want to forget it.quot; Also, serial killers seek perverse pleasure torturing the victim, even resuscitating them before they are about to die, so they can torture them more. John Wayne Gacy has been known to ask his victims, à ¢Ã¢â€š ¬Ã…“Howà ¢Ã¢â€š ¬Ã¢â€ž ¢s it feel knowing, your about to dieà ¢Ã¢â€š ¬? and then he strangles them to death. Serial killers need to dominate and à ¢Ã¢â€š ¬Ã…“ownà ¢Ã¢â€š ¬? their victims, yet the victims die; they are once alo ne again, and left with rage and self-hatred. There are six stages of the serial killers cycle; phase one-à ¢Ã¢â€š ¬Ã…“the aura phaseà ¢Ã¢â€š ¬?, where the killer loses grip on reality, phase two-à ¢Ã¢â€š ¬Ã…“the trolling phaseà ¢Ã¢â€š ¬?, when the killer searches for a victim, phase three-à ¢Ã¢â€š ¬Ã…“the wooing phaseà ¢Ã¢â€š ¬?, where the killer lures his victim, phase four-à ¢Ã¢â€š ¬Ã…“the captive phaseà ¢Ã¢â€š ¬?, when the victim is entrapped, phase five-à ¢Ã¢â€š ¬Ã…“the murderà ¢Ã¢â€š ¬?, which is the emotional high for the killer andShow MoreRelatedThe Mind and Motivation of a Serial Killer Essay777 Words   |  4 PagesThe mind and motivation of a serial killer Serial killers tend to be white heterosexual males in their twenties and thirties, who are sexually dysfunctional and have low self-esteem. Serial killers generally murder strangers with cooling off periods in between each murder. Serial killers are twisted in nature. Some return to the place the murder happened or the gravesite to fantasize about their deeds. 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