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group_5_presentation_3_-_anorexia [2018/03/30 23:48] colettj |
group_5_presentation_3_-_anorexia [2018/03/31 01:25] (current) bhattvj [Etiology] |
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| ====== Introduction ====== | ====== Introduction ====== | ||
| - | Anorexia is a life threatening mental illness that typically begins around puberty but can occur at any age. It is characterized by persistent behaviours that interfere with maintaining an adequate weight for health, a powerful fear of gaining weight or becoming fat, disturbance in how the person experiences their weight and shape and the individual not fully appreciating the seriousness of their condition. If these characteristics are seen over a period of a least three months an individual can be diagnosed with anorexia (Nedic, 2014). | + | Anorexia nervosa (AN) is a life threatening mental illness that typically begins around puberty but can occur at any age. It is characterized by persistent behaviours that interfere with maintaining an adequate weight for health, a powerful fear of gaining weight or becoming fat, disturbance in how the person experiences their weight and shape and the individual not fully appreciating the seriousness of their condition. If these characteristics are seen over a period of a least three months an individual can be diagnosed with anorexia (Nedic, 2014). |
| Persistent behaviours that interfere with maintaining an adequate weight for health includes: restricting food, compensating for food intake through intense exercise, and/or purging through self-induced vomiting or misuse of medications like laxatives, diuretics, enemas, or insulin. In the past anorexia used to be specifically associated with weight loss, making it difficult to recognize in children and adolescents. Weight gain is needed in children and adolescents in order to support healthy growth and development. Therefore, failing to gain weight or grow is just as concerning as weight loss (Nedic, 2014). | Persistent behaviours that interfere with maintaining an adequate weight for health includes: restricting food, compensating for food intake through intense exercise, and/or purging through self-induced vomiting or misuse of medications like laxatives, diuretics, enemas, or insulin. In the past anorexia used to be specifically associated with weight loss, making it difficult to recognize in children and adolescents. Weight gain is needed in children and adolescents in order to support healthy growth and development. Therefore, failing to gain weight or grow is just as concerning as weight loss (Nedic, 2014). | ||
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| ====== History ====== | ====== History ====== | ||
| - | Though not termed as anorexia nervosa, this condition has been seen since the Hellenistic era and has continued through the Middle Ages (Pini et al., 2016). During these times, it was focused on religious fasting, spiritual purity and self- sacrifice. The term, anorexia nervosa was first established by Sir William Gull in 1873; Sir William Gull made observations of this condition and presented it to the British Medical Association in Oxford, England (Pini et al., 2016). At the same time, French physician, Ernest- Charles Lasègue also published details of cases the same year that the term was created, his work concentrated more on the psychological symptoms and examined the role of parental and family interactions (Pini et al., 2016). Anorexia nervosa was the first eating disorder to be placed into the first DSM edition and it was not until 1980 that the body image disturbance criteria was a diagnostic criterion (Pini et al., 2016). In the DSM 5, it is now under the “other specified feeding or eating disorder” along with bulimia nervosa (BN), binge eating disorder (BED), avoidant/restrictive food intake disorder (ARFID), rumination disorder and pica (Pini et al., 2016). | + | Though not termed as anorexia nervosa at the beginning, this condition has been seen since the Hellenistic era and has continued through the Middle Ages (Pini et al., 2016). During these times, it was focused on religious fasting, spiritual purity and self- sacrifice. The term, anorexia nervosa was first established by Sir William Gull in 1873; Sir William Gull made observations of this condition and presented it to the British Medical Association in Oxford, England (Pini et al., 2016). At the same time, French physician, Ernest- Charles Lasègue also published details of cases the same year that the term was created, his work concentrated more on the psychological symptoms and examined the role of parental and family interactions (Pini et al., 2016). Anorexia nervosa was the first eating disorder to be placed into the first DSM edition and it was not until 1980 that the body image disturbance criteria was a diagnostic criterion (Pini et al., 2016). In the DSM 5, it is now under the “other specified feeding or eating disorder” along with bulimia nervosa (BN), binge eating disorder (BED), avoidant/restrictive food intake disorder (ARFID), rumination disorder and pica (Pini et al., 2016). |
| <box 50%| > {{ :anorexia_gull.png?200 |}} </box| | <box 50%| > {{ :anorexia_gull.png?200 |}} </box| | ||
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| Anorexia nervosa has no specific origin as it is difficult to separate whether the starvation causes the cascade in the body or whether it is the anorexia condition itself. Three major aspects have been highlighted as areas of special interest including the biology, psychology and environmental factors. | Anorexia nervosa has no specific origin as it is difficult to separate whether the starvation causes the cascade in the body or whether it is the anorexia condition itself. Three major aspects have been highlighted as areas of special interest including the biology, psychology and environmental factors. | ||
| - | Looking at the biology of the condition, it is seen that heritability can have a major influence in its development. The incidence rates of heritability can be influenced by from 50%-75% through various assessments (Bulik 2010). It should also be noted that there is no direct link of a gene affecting however a cascade if genes have not been identified. The serotonin pathway as described in the pathophysiology has been highlighted as a key factor in the progression of anorexia nervosa (Kaye et al. 2009). | ||
| - | The psychology behind the condition indicated that those with a tendency of obsessive-compulsive personality traits are individuals with an increased probability of developing this. Anorexia nervosa alleviates the propagation of anxious behaviours in lieu of a continuous fear of food and gaining weight (Rothenburg 1988). | + | Looking at the biology of the condition, it is seen that heritability can have a major influence in its development. The incidence rates of heritability can be influenced by from 50%-75% through various assessments (Bulik, 2010). It should also be noted that there is no direct link of a gene affecting however a cascade if genes have not been identified. The serotonin pathway as described in the pathophysiology has been highlighted as a key factor in the progression of anorexia nervosa (Kaye et al., 2009). |
| - | Environmental factors, especially through the influence of western culture, drives the desire to be thin as it represents success and worth. The media often perpetuates a culture of continuous scrutiny over one’s body, idolizing the thin (Mayo Clinic). | + | The psychology behind the condition indicated that those with a tendency of obsessive-compulsive personality traits are individuals with an increased probability of developing this. Anorexia nervosa alleviates the propagation of anxious behaviours in lieu of a continuous fear of food and gaining weight (Rothenburg, 1988). |
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| + | Environmental factors, especially through the influence of western culture, drives the desire to be thin as it represents success and worth. The media often perpetuates a culture of continuous scrutiny over one’s body, idolizing the thin (Mayo Clinic, 2018). | ||
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| Some common symptoms for patients with anorexia are: extreme weight loss, fatigue, insomnia, dizziness or insomnia, constipation and abdominal pain, low blood pressure, and dehydration. Lastly, some patients present with bulimic symptoms - binging and purging ("Anorexia nervosa - Symptoms and causes", 2018). | Some common symptoms for patients with anorexia are: extreme weight loss, fatigue, insomnia, dizziness or insomnia, constipation and abdominal pain, low blood pressure, and dehydration. Lastly, some patients present with bulimic symptoms - binging and purging ("Anorexia nervosa - Symptoms and causes", 2018). | ||
| + | Several complications can arise from AN including gastrointestinal, cardiovascular, pulmonary and skeletal system complications (Mitchell & Crow, 2006). Gastric dilation, mucosal necrosis, delayed gastric emptying, gastric motor dysfunction, constipation, pancreatitis, and perforated ulcers (Mitchell & Crow, 2006). Cardiovascular complications include arrhythmias, acrocyanosis, tachycardia, bradycardia, and hypotension (Mitchell & Crow, 2006). Lastly, skeletal complications include decreased bone mineral density, which leads to osteopenia and other bone- related complications (Mitchell & Crow, 2006). | ||
| <box 50%| > {{ :anorexia-symptoms.jpg?300 |}} </box| Figure 7: This figure shows the symptoms that people with anorexia may present with. > | <box 50%| > {{ :anorexia-symptoms.jpg?300 |}} </box| Figure 7: This figure shows the symptoms that people with anorexia may present with. > | ||
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| ====== Current Treatments ====== | ====== Current Treatments ====== | ||
| - | Unfortunately today there are no treatments for Progeria. Physicians and healthcare providers’ main goals right now are to delay or reduce symptoms. This can be achieved by: small doses of aspirin, preventative medications, physical and occupational therapy, nutrition and dental care. Common with Progeria, small doses of Aspirin attempt to reduce the risk of heart attacks and strokes. Preventative medications that can help lower cholesterol, blood pressure, and reduce the chance of getting a blood clot can all be prescribed if the individual seems to be at risk. Physical and occupational therapy can help an individual maintain healthy movement capability and nutrition and dental care for being overall healthy (Mayo Clinic, 2018). Progeria is commonly screened phenotypically or through medical history at the physician’s office. A genetic test for the LMNA mutations can be ordered if the physician deems this appropriate (Sinha, Raghunath & Ghosh, 2018). | + | Through research, it is clearly exemplified that anorexia nervosa is merely not an eating disorder but dives into deep-seeded issues an individual may have. The first step includes the acceptance of their disorder and familial assistance prepares individuals for the upcoming services. |
| + | A psychiatrist is beneficial for the prescription of medications including antidepressants as several individuals experience anxiety in accordance with the eating disorder (Kaye et. al 1999). Enlisting the services of a nutritionist will be of benefit as managing the fear of food will be adequately guided by a professional ensuring the appropriate quality and quantities of food are provided. | ||
| <box 70%| > {{ :anorexia_treatment.png?300 |}} </box| Figure 11: This image compiles a list of services an individual with anorexia nervosa may use to treat the condition. > | <box 70%| > {{ :anorexia_treatment.png?300 |}} </box| Figure 11: This image compiles a list of services an individual with anorexia nervosa may use to treat the condition. > | ||
| - | For potential future treatments, there are many different angles of approach. Genetics currently is a big area of research for this disease. Anything from early detection capability, to actual cures, genetics is a significant field to target. Additionally, there is also a lot of interest in reducing the severity of symptoms, common with individuals with Progeria. First, heart and blood vessel disease is a target of interest. Farnesyltransferase inhibitors (FTIs), which are drugs for treating cancer, are being investigated to whether they can help vasodilate blood vessels and reduce weight gain (Mayo Clinic, 2018). In 2012, 25 children with Progeria underwent a clinical trial that showed these results (Gordon et al., 2012). FTIs also have shown in mouse models to improve nuclear shape and reduce the negative effects of built up prelamin A. Lonafarnib, an FTI, certainly gives confidence for developing a potential cure to Progeria (Sinha, Raghunath & Ghosh, 2018). | + | The implementation of cognitive behavioural therapy will use psychotherapy as a means to address the underlying thoughts behind the condition. This will recognize those symptoms and assist in a healthy method of alleviating those notions (Kaye et al. 1999). Managing a long term eating disorder will be a difficult challenge however with the enlistment of these services, recovery will be possible. |
| - | (a is Progerin cell, d is a healthy cell - treated with FTI - Capell reference) | + | |
| ======Conclusion====== | ======Conclusion====== | ||
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| Anorexia Nervosa-What Increases Your Risk. (2018). WebMD. Retrieved 26 March 2018, from https://www.webmd.com/mental-health/eating-disorders/anorexia-nervosa/anorexia-nervosa-what-increases-your-risk | Anorexia Nervosa-What Increases Your Risk. (2018). WebMD. Retrieved 26 March 2018, from https://www.webmd.com/mental-health/eating-disorders/anorexia-nervosa/anorexia-nervosa-what-increases-your-risk | ||
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| Bulik CM, Thornton LM, Root TL, et al. Understanding the relation between anorexia nervosa and bulimia nervosa in a Swedish national twin sample. Biol Psychiatry. 2010;67:71-77. | Bulik CM, Thornton LM, Root TL, et al. Understanding the relation between anorexia nervosa and bulimia nervosa in a Swedish national twin sample. Biol Psychiatry. 2010;67:71-77. | ||
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| Fairburn, C., Cooper, Z., Doll, H., & Welch, S. (1999). Risk Factors for Anorexia Nervosa. Archives Of General Psychiatry, 56(5), 468. http://dx.doi.org/10.1001/archpsyc.56.5.468 | Fairburn, C., Cooper, Z., Doll, H., & Welch, S. (1999). Risk Factors for Anorexia Nervosa. Archives Of General Psychiatry, 56(5), 468. http://dx.doi.org/10.1001/archpsyc.56.5.468 | ||
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| + | Kaye, W., Strober, M., Stein, D., & Gendall, K. (1999). New directions in treatment research of anorexia and bulimia nervosa. Biological Psychiatry, 45(10), 1285-1292. | ||
| Keski-Rahkonen, A., Hoek, H. W., Susser, E. S., Linna, M. S., Sihvola, E., Raevuori, A., ... & Rissanen, A. (2007). Epidemiology and course of anorexia nervosa in the community. American Journal of Psychiatry, 164(8), 1259-1265. | Keski-Rahkonen, A., Hoek, H. W., Susser, E. S., Linna, M. S., Sihvola, E., Raevuori, A., ... & Rissanen, A. (2007). Epidemiology and course of anorexia nervosa in the community. American Journal of Psychiatry, 164(8), 1259-1265. | ||
| Micali, N., Hagberg, K. W., Petersen, I., & Treasure, J. L. (2013). The incidence of eating disorders in the UK in 2000–2009: findings from the General Practice Research Database. BMJ Open, 3(5). | Micali, N., Hagberg, K. W., Petersen, I., & Treasure, J. L. (2013). The incidence of eating disorders in the UK in 2000–2009: findings from the General Practice Research Database. BMJ Open, 3(5). | ||
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| + | Mitchell, J. E., & Crow, S. (2006). Medical complications of anorexia nervosa and bulimia nervosa. Current Opinion in Psychiatry, 19(4), 438-443. | ||
| Nedic. (2018). National Eating Disorder Information Center. Nedic.ca. Retrieved 24 March 2018, from http://nedic.ca/know-facts/overview | Nedic. (2018). National Eating Disorder Information Center. Nedic.ca. Retrieved 24 March 2018, from http://nedic.ca/know-facts/overview | ||
