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| ====== Anorexia ====== | ====== Anorexia ====== | ||
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| {{ :powerpoint-anorexia-1-728.jpg?300 |}} | {{ :powerpoint-anorexia-1-728.jpg?300 |}} | ||
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| - | ====== Overview ====== | + | ======= Overview ======= |
| - | ==== 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 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| | ||
| + | Figure 1: Sir William Gull, an English physician that established the term anorexia nervosa. > | ||
| - | Progeria is an extremely rare genetic disease of childhood characterized by dramatic, premature aging with death occurring on average at the age of 13, usually from heart attack or stroke (Kashyap et al., 2014). Hutchinson-Gilford progeria syndrome (HGPS) is the most severe form of the disease and the classic type. The disease was named after the doctors who first described it in England; in 1886 by Dr. Jonathan Hutchinson and in 1897 by Dr. Hastings Gilford. The term progeria is derived from the Greek work geras, meaning old age (DeBusk, 1972). | + | <box 50%| > {{ :anorexia_miss_a.png?200 |{{ :screen_shot_2018-03-02_at_3.52.34_am.png?300 |}} </box| Figure 2: “ Miss A” one of the earliest cases pictured in 1866 and in 1870 after treatment of anorexia nervosa as published by the medical papers of Sir William Gull > |
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| - | In 1886, the syndrome was first reported by Hutchinson of a 6-year-old boy whose overall appearance was that of an old man. Hutchinson described the case as “congenital absence of hair and its appendages” (DeBusk, 1972). It was a year later that Gilford described a second patient with similar clinical findings. To date, there are only 100 patients with HGPS that have been described in literature (Kashyap et al., 2014). These two boys were further described in 1897 and 1904 by Gildford, who was the one to proposal the term “progeria” and described the post-mortem characteristics (DeBusk, 1971). Little research was done on the disease until the 1990’s due to the rarity of the disease, causing it to be frequently diagnosed erroneously in patients with some of the features such as alopecia and skin of aged appearance (DeBusk, 1972). However, there are three features present in early life; mid-facial cyanosis, skin resembling scleroderma, and glyphic nasal tip, which all facilitate an early diagnosis of HGPS (DeBusk, 1972). | + | ====== Etiology ====== |
| + | |||
| + | 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. | ||
| - | <box 80%| > {{ :screen_shot_2018-03-02_at_3.52.29_am.png?300 |}} </box| | + | 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). |
| - | Figure 1: Dr. Jonathan Hutchinson was the first doctor to describe a case of progeria in 1886. | + | |
| - | > | + | |
| - | <box 80%| > {{ :screen_shot_2018-03-02_at_3.52.34_am.png?300 |}} </box| Figure 2: Dr. Hastings Gilford described the second case of progeria in 1887. He was the individual to purpose the term progeria and describe the post-mortem characteristics. > | + | 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). |
| + | 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). | ||
| ====== Epidemiology ====== | ====== Epidemiology ====== | ||
| - | HPGS is an extremely rare genetic disorder affecting about 1 in 4 million live births, if unreported or misdiagnosed cases are taken into account. The reported prevalence rate of the disease is 1 in 8 million births, based on the number of cases (Coppedè, 2013). According to the Progeria Research Foundation database, there are an estimated 350-400 children living with progeria worldwide at any one time. As of January 2018, there are a recorded 114 children living with progeria worldwide with numbers steadily increasing as the years go by (http://www.progeriaresearch.org/prf-by-the-numbersprf.html). | + | The lifetime prevalence, incidence rates and 5 year recovery rates were calculated from data from 2882 women from 1975-1979 birth cohorts of Finnish twins (Keski-Rahkonen et al., 2007). The incidence in women aged 15 to 19 years was 270 per 100,000 person- years (Keski-Rahkonen et al., 2007). The 5 year clinical recovery rate was 66.8% at which complete or nearly complete psychological recovery was seen (Keski-Rahkonen et al., 2007). Western countries have a higher prevalence than non- Western countries (Keski-Rahkonen et al., 2007). |
| - | HPGS affects all races; cases of progeria have been discovered in 45 different countries. However, 97% of affected patients are white. Males are affected 1 ½ times more often than females. The disease was thought to be autosomal recessive in the past, however observations made an autosomal recessive inheritance very unlikely and favour a sporadic, dominant mutation. The mutation results in life spans for progeria syndrome to be in the second/third decades of life, with the majority of patients dying of cardiovascular or cerebrovascular disease between 7 and 27 years of age (Sarkar and Shinton, 2001). | + | The average prevalence in Western Europe and North America is 0.3% (National Eating Disorder Information Centre, 2018) . The lifetime prevalence in females is 0.9% and in males is 0.3%; note lifetime prevalence is defined as the proportion of individuals in a population that at some point in their life have experienced the disease (National Eating Disorder Information Centre, 2018). The prevalence of AN in Canada is 0.3% in adolescent and young women (National Eating Disorder Information Centre, 2018). |
| - | <box 80%| > {{ :screen_shot_2018-03-02_at_4.02.11_am.png?300 |}}</box| Figure 3: Number of children and countries that PRF has identified with cases of progeria over the years. > | ||
| - | <box 80%| > {{ :screen_shot_2018-03-02_at_4.02.19_am.png?300 |}} </box| Figure 4: The 45 different countries that PRF has identified with cases of progeria as of January 1st, 2018. > | + | <box 70%| > {{ :anorexia_incidence_rates.png?600 |}} </box| Figure 3: Incidence rates and 95% confidence intervals of anorexia nervosa (AN), bulimia nervosa (BN) and eating disorder not otherwise specified (EDNOS) by year for females aged 10- 49 years in the UK. > |
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| + | <box 70%| > {{ :anorexia_incidence_rates_male.png?600 |}} </box| Figure 4: Incidence rates and 95% confidence intervals of anorexia nervosa (AN), bulimia nervosa (BN) and eating disorder not otherwise specified (EDNOS) by year for males aged 10- 49 years in the UK. > | ||
| ==== Risk Factors ==== | ==== Risk Factors ==== | ||
| It has been found that there are several risk factors for developing anorexia. These include: perfectionism, negative self-evaluation, obesity, family history of anorexia, affective disorder, substance abuse, obsessive-compulsive disorder and a stress/trigger. It was also found that a lot of these risk factors were correlated to being risk factors of other psychological conditions and that they could have been acquired genetically (Fairburn, Cooper, Doll & Welch, 1999). It should also be mentioned that all of the aforementioned risk factors are not known in detail - their significance is unknown at this point. Social determinants, culture and family also play a role, and vary significantly ("Anorexia Nervosa-What Increases Your Risk", 2018). | It has been found that there are several risk factors for developing anorexia. These include: perfectionism, negative self-evaluation, obesity, family history of anorexia, affective disorder, substance abuse, obsessive-compulsive disorder and a stress/trigger. It was also found that a lot of these risk factors were correlated to being risk factors of other psychological conditions and that they could have been acquired genetically (Fairburn, Cooper, Doll & Welch, 1999). It should also be mentioned that all of the aforementioned risk factors are not known in detail - their significance is unknown at this point. Social determinants, culture and family also play a role, and vary significantly ("Anorexia Nervosa-What Increases Your Risk", 2018). | ||
| - | <box 80%| > {{ :eatingdisorders-300x281.jpg?300 |}} </box| Figure 5: The main 3 categories of risk factors of anorexia. > | + | <box 50%| > {{ :eatingdisorders-300x281.jpg?300 |}} </box| Figure 5: The main 3 categories of risk factors of anorexia. > |
| - | <box 80%| > {{ :picture-11.png?300 |}} </box| Figure 6: Perfectionism is a major risk factor for developing anorexia. > | + | <box 50%| > {{ :picture-11.png?300 |}} </box| Figure 6: Perfectionism is a major risk factor for developing anorexia. > |
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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 70%| > {{ :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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| Although AN is characterized as an eating disorder, it remains unknown whether there is a primary disturbance of appetitive pathways, or whether there could be other causes such as anxiety or obsessive preoccupation with weight gain. | Although AN is characterized as an eating disorder, it remains unknown whether there is a primary disturbance of appetitive pathways, or whether there could be other causes such as anxiety or obsessive preoccupation with weight gain. | ||
| - | <box 70%| > {{ :anorexia-symptoms.jpg?300 |}} </box| Figure 8: If they have a personality or temperament predisposition trait it can contribute to one’ vulnerability of developing anorexia. It is usually seen that it becomes intensified during adolescence. > | + | <box 70%| > {{ :anorexia_patho1.png?500 |}} </box| Figure 8: If they have a personality or temperament predisposition trait it can contribute to one’ vulnerability of developing anorexia. It is usually seen that it becomes intensified during adolescence. > |
| === Serotonin Function === | === Serotonin Function === | ||
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| The 5-HT serotonin system has been studied in individuals that have AN, to suggest that it is possible that this neurotransmitter system plays a role in many symptoms of anorexia such as enhanced satiety, impulse control and mood. | The 5-HT serotonin system has been studied in individuals that have AN, to suggest that it is possible that this neurotransmitter system plays a role in many symptoms of anorexia such as enhanced satiety, impulse control and mood. | ||
| - | <box 70%| > {{ :anorexia-symptoms.jpg?300 |}} </box| Figure 9: Individuals that are more vulnerable to the development of an eating disorder may have an imbalance in the postsynaptic 5-HT(1A) and 5-HT(2) receptor activity (Kaye et al, 2009). > | + | <box 70%| > {{ :anorexia_patho2.png?600 |}} </box| Figure 9: Individuals that are more vulnerable to the development of an eating disorder may have an imbalance in the postsynaptic 5-HT(1A) and 5-HT(2) receptor activity (Kaye et al, 2009). > |
| It has been said that these might contribute to an increase in satiety and a more anxious harm-avoidant temperament. Individuals with Anorexia are said to have a reduction in dysphoric mood. Starvation is associated with an increase in postsynaptic 5-HT1A receptor binding potential. Additionally the binding of the 5-HT-2A receptor is positively correlated with harm avoidance in individuals that suffer from AN (Kaye et al, 2009). Individuals with AN will usually pursue starvation ass an attempt to avoid the dysphoric mood that comes as a consequence due to this increased stimulation of postsynaptic 5-HT1A and 5-HT2A receptors and therefore makes eating and weight gain aversive (Kaye et al , 2009). | It has been said that these might contribute to an increase in satiety and a more anxious harm-avoidant temperament. Individuals with Anorexia are said to have a reduction in dysphoric mood. Starvation is associated with an increase in postsynaptic 5-HT1A receptor binding potential. Additionally the binding of the 5-HT-2A receptor is positively correlated with harm avoidance in individuals that suffer from AN (Kaye et al, 2009). Individuals with AN will usually pursue starvation ass an attempt to avoid the dysphoric mood that comes as a consequence due to this increased stimulation of postsynaptic 5-HT1A and 5-HT2A receptors and therefore makes eating and weight gain aversive (Kaye et al , 2009). | ||
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| Individuals who have AN will usually experience an aversive visceral sensation when they are exposed to food or a form of food-related stimuli. This creates a bias towards the reward-related properties of food and creates a more negative emotion. This minimizes the exposure to food stimuli (Kaye et a, 2009). | Individuals who have AN will usually experience an aversive visceral sensation when they are exposed to food or a form of food-related stimuli. This creates a bias towards the reward-related properties of food and creates a more negative emotion. This minimizes the exposure to food stimuli (Kaye et a, 2009). | ||
| - | <box 70%| > {{ :anorexia-symptoms.jpg?300 |}} </box| Figure 10: The different effects of the presentation of food in individuals who are healthy and individuals with anorexia nervosa. > | + | <box 70%| > {{ :anorexia_patho3.png?500 |}} </box| Figure 10: The different effects of the presentation of food in individuals who are healthy and individuals with anorexia nervosa. > |
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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. | ||
| - | 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). | + | |
| - | (a is Progerin cell, d is a healthy cell - treated with FTI - Capell reference) | + | <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. > |
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| + | 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. | ||
| ======Conclusion====== | ======Conclusion====== | ||
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| Anorexia nervosa - Symptoms and causes. (2018). Mayo Clinic. Retrieved 26 March 2018, from https://www.mayoclinic.org/diseases-conditions/anorexia/symptoms-causes/syc-20353591 | Anorexia nervosa - Symptoms and causes. (2018). Mayo Clinic. Retrieved 26 March 2018, from https://www.mayoclinic.org/diseases-conditions/anorexia/symptoms-causes/syc-20353591 | ||
| - | Diagnosis of anorexia nervosa. (2018). Healthdirect.gov.au. Retrieved 26 March 2018, from https://www.healthdirect.gov.au/diagnosis-of-anorexia-nervosa | + | 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 |
| - | Rothenberg, A. (1988). Differential diagnosis of anorexia nervosa and depressive illness: A review of 11 studies. Comprehensive Psychiatry, 29(4), 427-432. http://dx.doi.org/10.1016/0010-440x(88)90024-7 | + | 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. |
| + | Dell’Osso, L., Abelli, M., Carpita, B., Pini, S., Castellini, G., Carmassi, C., & Ricca, V. (2016). Historical evolution of the concept of anorexia nervosa and relationships with orthorexia nervosa, autism, and obsessive–compulsive spectrum. Neuropsychiatric disease and treatment,12, 1651. | ||
| - | 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 | + | Diagnosis of anorexia nervosa. (2018). Healthdirect.gov.au. Retrieved 26 March 2018, from https://www.healthdirect.gov.au/diagnosis-of-anorexia-nervosa |
| 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 | ||
| - | 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). | + | 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. |
| - | + | ||
| - | Dell’Osso, L., Abelli, M., Carpita, B., Pini, S., Castellini, G., Carmassi, C., & Ricca, V. (2016). Historical evolution of the concept of anorexia nervosa and relationships with orthorexia nervosa, autism, and obsessive–compulsive spectrum. Neuropsychiatric disease and treatment,12, 1651. | + | |
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| 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. | ||
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| + | 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. | ||
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| + | Nedic. (2018). National Eating Disorder Information Center. Nedic.ca. Retrieved 24 March 2018, from http://nedic.ca/know-facts/overview | ||
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| + | Rothenberg, A. (1988). Differential diagnosis of anorexia nervosa and depressive illness: A review of 11 studies. Comprehensive Psychiatry, 29(4), 427-432. http://dx.doi.org/10.1016/0010-440x(88)90024-7 | ||
| Statistics | National Eating Disorder Information Centre (NEDIC). (2018). Nedic.ca. Retrieved 24 March 2018, from http://nedic.ca/node/24 | Statistics | National Eating Disorder Information Centre (NEDIC). (2018). Nedic.ca. Retrieved 24 March 2018, from http://nedic.ca/node/24 | ||
