16 Eating disorders
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1. Parental discord has an aetiological role in the genesis of eating disorder. | ![]() |
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2. EAT is a self-rated questionnaire. | ![]() |
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3. Cholecystokinin in the gastrointestinal tract hinders satiety. | ![]() |
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4. Insulin release from the pancreas after a carbohydrate meal reduces the ratio of tryptophan/large amino acids. | ![]() |
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5. Paraventricular 5-HT nuclei are responsible for satiety. | ![]() |
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6. Leptin level increases in proportion to body mass index. | ![]() |
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7. Over 50% of girls in developed countries engage in abnormal eating. | ![]() |
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8. Enmeshment is a feature of families of patients with anorexia nervosa. | ![]() |
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9. T4 is increased in anorexia. | ![]() |
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10. Anorexia nervosa patients adopt the sick role. | ![]() |
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11. In treatment of anorexic patients with severe weight loss, initial weight gain is associated with cognitive improvement. | ![]() |
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12. Anorexia can be prevented by education in schools, activities and peer focus group discussions. | ![]() |
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13. Family therapy is more effective than individual therapy for younger patients with anorexia nervosa. | ![]() |
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14. In anorexia, late onset predicts poor outcome. | ![]() |
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15. Vomiting is a positive prognostic factor in anorexia nervosa. | ![]() |
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16. In anorexia nervosa, earlier onset is a good prognostic factor. | ![]() |
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17. In anorexia the mortality rate is 5% per year. | ![]() |
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18. In anorexia family turmoil predicts poor outcome. | ![]() |
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19. Short time from onset to presentation is a good prognostic factor for anorexia nervosa. | ![]() |
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20. Bulimia nervosa is associated with shoplifting. | ![]() |
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21. Menstrual irregularities are frequent in bulimia nervosa. | ![]() |
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22. In bulimia there is a risk of seizures. | ![]() |
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23. In bulimia nervosa, cognitive therapy (CBT) and interpersonal therapy (IPT) are equally effective. | ![]() |
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24. Bulimia is associated with increased mortality. | ![]() |
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25. Bulimia is associated with an increased risk of rectal carcinoma. | ![]() |
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ANSWERS
True: Family discord and life events such as parental separation have been associated with the onset of eating disorders. However, no single specific family functioning style appears to be necessary or sufficient for the development of eating disorders. As in most psychiatric disorders, dysfunctional family styles may act as non-specific vulnerability factors and may hamper recovery. Family disturbances seem to increase with the duration of the disorder, suggesting that the disorder causes family disturbance rather than vice versa. However, they are useful for developing working understandings of how certain family patterns may perpetuate the illness (Gelder et al 2006, p. 363; Johnstone et al 2004, p. 494; Sadock & Sadock 2005, p. 2008; Wright et al 2005, p. 222).
True: Eating Attitudes Test is a self-rated questionnaire. Other self-reported questionnaires include Eating Disorders Investigation (EDI) and the Bulimic Investigatory Test, Edinburgh (BITE). Eating Disorders Examination (EDE) is a structured interview. The Morgan–Russell scales assess physical and psychological status (Wright et al 2005, p. 218).
False: Cholecystokinin (CCK) is a gut peptide released from the gastrointestinal tract by the local action of digested food that controls meal size in humans and animals. A blunted postprandial CCK release is associated with impaired satiety, e.g. in bulimics. Receptors that initiate CCK’s satiating action are located in the proximal small intestine, not in the brain. Activation of these receptors increases the activity of the vagal afferents innervating this site. Transection of the vagal afferent fibres abolishes the satiating action of CCK (Puri & Tyrer 1998, p. 61; Sadock & Sadock 2005, p. 299; Wright et al 2005, p. 232).
False: Insulin release leads to an increase in the plasma concentration of tryptophan and a reduction in large neutral amino acid (LNAA) concentrations. This increases the tryptophan/LNAA ratio (Virkkunen & Narvanen 1987).
True: 5-HT inhibits feeding and promotes satiety. Paraventricular, ventromedial and suprachiasmatic nuclei mediate satiety through 5-HT (Gelder et al 2000, p. 840; Wright et al 2005, p. 232).
True: Leptin is called the ‘satiety hormone’. Leptin is secreted by adipose tissue. Plasma leptin levels are closely correlated with body fat mass and increase in proportion to the body mass index. Leptin is transported across the blood–brain barrier to various brain loci. It acts in the brain to inhibit eating and to stimulate energy expenditure by increasing physical activity (Gelder et al 2000, p. 868; Sadock & Sadock 2005, p. 300).
False: In a recent US study, up to 26% of female students and 10% of male students had engaged in abnormal eating or weight control measures over the previous month (Forman-Hoffman 2004).
True: A specific pattern of family relationships consisting of ‘enmeshment, overprotectiveness, rigidity and lack of conflict resolution’ was hypothesized to increase the chance of a daughter developing anorexia. However, no single specific family functioning style appears to be necessary or sufficient for the development of eating disorders. These features of family function are not unique to families of anorexics (Gelder et al 2006, p. 363; Johnstone et al 2004, p. 494; Sadock & Sadock 2005, p. 2008).
False: Thyroxine (T4) and TSH are usually normal. T3 is often reduced. TSH response to TRH is blunted (Gelder et al 2000, p. 842; Gelder et al 2006, p. 361; Johnstone et al 2004, p. 492).
False: Parsons (1951) described the features of sick role. They include:
Patients with anorexia nervosa do not adopt the sick role but engage in what
Pilowsky (1969) called abnormal illness behaviour or dysnosognosia, i.e. persistently pathological modes of experiencing, evaluating and responding to one’s own health status despite lucid and accurate appraisal and management options provided by health professionals (Gelder et al 2006, p. 165; Murray et al 1997, pp. 51, 483; Stein & Wilkinson 1998, p. 719;).True: Weight restoration results in an improvement in cognitive functioning. Attention improves first, followed by memory, visuospatial functioning and learning (Szmukler et al 1995, p. 205).
False: There is very little evidence to support this (Pratt & Woolfenden 2002).
True: Family therapy has been shown to be more effective than individual supportive psychotherapy for patients with onset before age 19 years and duration less than 3 years. However, patients with late onset anorexia do better with individual supportive psychotherapy than with family therapy (Gelder et al 2000, p. 849; Johnstone et al 2004, p. 495; Wright et al 2005, p. 224).
True: In anorexia, older age of onset, i.e. above 15 years, is a poor prognostic factor. Other poor prognostic factors include lower minimum weight, longer duration of illness (>6–10 yrs), poor relationship with family, personality difficulties, social problems, premorbid obesity, bulimic behaviour and male gender (Gelder et al 2000, p. 847; Stein & Wilkinson 1998, p. 883; Wright et al 2005, p. 230).
False: Patients with the bingeing/purging subtype of anorexia have a poorer prognosis. This is consistent with the original description by Russell (1979) of bulimia nervosa as an ‘ominous variant’ of anorexia nervosa (Wright et al 2005, p. 230).
True: Those who develop anorexia before the age of 15 years have a better prognosis (Gelder et al 2000, p. 847; Stein & Wilkinson 1998, p. 883; Wright et al 2005, p. 230).
False: The mortality rate in anorexia nervosa is estimated to be 0.59% per year. The mortality is higher amongst those with weight less than 35 kg. The standardized mortality rate is 6 times that of the general population (Stein & Wilkinson 1998, p. 884; Szmukler et al 1995, p. 198; Treasure & Schmidt 2005; Wright et al 2005, p. 230).
True: Relationship difficulties within the family are a poor prognostic factor (Gelder et al 2000, p. 846; Wright et al 2005, p. 230).
True: Favourable prognostic factors include earlier age of onset and shorter interval between onset and treatment (Stein & Wilkinson 1998, p. 883; Treasure & Schmidt, 2005; Wright et al 2005, p. 230).
True: A minority of bulimia sufferers have ‘multi-impulsive behaviours’. They include repeated self-harm, alcohol and drug misuse, sexual promiscuity, shoplifting and other self-damaging behaviours. 10–50% of patients admit to stealing food to binge on (Johnstone et al 2004, p. 496; Sadock & Sadock 2002, p. 747; Wright et al 2005, p. 231).
True: Unlike anorexia, amenorrhoea is not necessary for the diagnosis. Up to 60% of bulimics experience loss of ovulation and irregular menstruation or amenorrhoea. An association with polycystic ovaries has also been identified (Gelder et al 2000, p. 859; Johnstone et al 2004, p. 497; Wright et al 2005, p. 220).
True: Generalized seizures are a recognized complication of electrolyte disturbance and large fluid shifts caused by bingeing and vomiting (Johnstone et al 2004, p. 492; Sadock & Sadock 2002, p. 742).
False: At the end of treatment both IPT and CBT result in similar improvement in abstinence from both binge eating and purging. However, at 1 year follow-up, the improvement is better maintained in those who had CBT. CBT is the preferred treatment for bulimia. IPT is an efficacious alternative but may take up to 8–12 months longer to achieve the same results (Hay & Bacaltchuk 2004; NICE).
False: Unlike anorexia the mortality rate is not raised in bulimia (0.3–1.1%). The prognosis is better than for anorexia. The illness runs a relapsing and remitting course with recovery rates between 50 and 70%. At 10-year follow-up about 10% remain bulimic and 15% meet the criteria for an atypical eating disorder (Gelder et al 2000, p. 865; Johnstone et al 2004, p. 493; Stein & Wilkinson 1998, p. 895; Wright et al 2005, p. 235).
False: Bulimia does not increase the risk of rectal carcinoma. Recognized gastrointestinal problems include constipation, cathartic colon, damaged myenteric plexus, gastric and duodenal ulcers, oesophageal erosions, gastric perforation, irritable bowel and pancreatitis (Johnstone et al 2004, p. 492; Sadock & Sadock 2005, p. 2016).