Ma Cristy L.

Exconde, MD, FPOGS

Roadmap
Anorexia Nervosa Diagnosis
Bulemia Nervosa Epidemiology
Binge-eating disorder Medical risks
Obesity Etiology
Treatment
prognosis
Risk Factors for EDs
Perfectionism for AN
Early Puberty
Failed attempts to lose weight
Athletics
Beginning a diet
Family history of eating disorder, substance abuse or
mood disorder
Diagnosis AN (DSM-5):
 Restriction of energy intake relative to
requirements leading to a significantly low body
weight in the context of age, sex.
 Intense fear of gaining weight or becoming fat,
or persistent behavior that interferes
with weight gain.
Disturbance in one's body weight or shape ,
persistent lack of recognition of the seriousness
of low body weight
Specify:
Restricting type
Purging type/Binge Eating.
Subtypes AN (DSM-5):

Restricting Type: during last 3months, the person has

not engaged in recurrent episodes of binge eating or
purging behavior
Binge-Eating/Purging Type: during last 3 months, the
person engaged in
recurrent episodes of binge eating or purging behavior
Epidemiology:
Life time prevalence 0.5- 3.7%
 Girls from 14- 18ys 0.5- 1%
AN and BN 30 - 50%
Death 3-8%
Age: 10-30years.
Risk : Sp. After stress
M:F ratio 1: 20
In professions modeling –
ballet dancers.
Medical Complication
Death (hypokalemia , starvation, sudden cardiac
death)
Hypometabolic state (bradycardia, hypotension,
hypothermia)
Dehydration
Arrhythmia, heart failure.
Bone loss
Peripheral edema
Delayed sexual maturity
Hair loss, brittle hair, Lanugo.
On recovery: Re-feeding syndrome
Etiology

(kristinaschwerin
et.al.2010)
Etiology and Pathophysiology
 Exact etiology is unknown
 Combination of genetic, biologic, developmental
and environmental factors
 AN linked with enlarge cortical sulci, ventricles and
interhemospheric fissure
 AN linked with reductions in gray matter
(amygdala, hippocampus, putamen, cingulate
cortex)
Diagnostic Criteria and Clinical
Presentation
 Clinical Presentation
• Anorexia Nervosa General
• Restriction of energy intake that leads to low body weight and self-
evaluation that is influenced by perceptions of weight and body shape.
• Symptoms
• Patients have obsessions and fears about eating and gaining weight.
• They complain about feeling full even when they have eaten very little
food.
• Denial of symptoms, failure to recognize low body weight, and low self-
esteem.
• Patients often feel ineffective and have a lack of self-control.
• Signs
• Weakness, lethargy, cachexia, amenorrhea, vomiting, restricted food
intake, inappropriate exercise, delayed sexual development, edema,
delayed gastric emptying, constipation, abdominal pain, bradycardia,
hypotension, osteoporosis, dry cracking skin, lanugo, callus on dorsum
of hand, cold intolerance, perioral dermatitis, and erosion of dental
enamel.
 Clinical Presentation
• Laboratory Abnormalities
• Hypokalemia, hypochloremia, hypothyroidism,
hypophosphatemia, hypokalemic alkalosis,
hypomagnesemia, metabolic acidosis, blood urea
nitrogen, hepatic enzymes, leukopenia,
thrombocytopenia, anemia, QT interval prolongation,
bradycardia, hypercholesterolemia, and bone mineral
density.
• Other Diagnostic Tests
• Nonspecific electroencephalogram (EEG) change
 Clinical Presentation
• Bulimia Nervosa General
• Patients binge eat and stop when they have abdominal
pain or self-induced vomiting or are interrupted by
another person.
• They have a pattern of severe dieting followed by
binge eating episodes.
• They are concerned about their body image but do not
have the drive to thinness, which is a characteristic of
AN.
 Clinical Presentation
• Symptoms
• Patients do not eat regular meals and do not feel satiety
at the end of a meal.
• They may use purging methods such as laxatives for
weight control.
• They have guilt, depression, and self-disparagement
after binges.
• Social isolation can result from frequent bingeing.
• Chaotic and troubled personal relationships and
substance abuse are common.
 Clinical Presentation
• Signs
• Bingeing, vomiting, salivary gland inflammation,
erosion of dental enamel, callus on dorsum of hand,
perioral dermatitis, dental caries, parotid gland
enlargement, abdominal pain, upper end of normal
body weight or slightly overweight, frequent weight
fluctuations, and diminished masticatory ability.
 Clinical Presentation
• Laboratory Abnormalities
• Hypokalemia, hypochloremic metabolic
acidosis, and elevated serum amylase.
• Other Diagnostic Tests
• None
 Clinical Presentation
• Binge-Eating Disorder
• Patients with BED present with recurrent episodes of
bingeing without the compensatory behaviors
associated with AN or BN.
• It is estimated that 5% to 10% of patients seeking
treatment for obesity have BED.
• Comorbid psychotic disorders are common and
reported in greater than 70% of BED patients.
• Depression and low self-esteem are common, but self-
deprecating focus on body image is less severe than in
AN or BN.
 Clinical Presentation
• Diagnostic criteria for BED requires
recurrent episodes of binge eating
(eating an amount of food in a specific
period of time that is larger than what
most people would eat in a similar
situation and a sense of lack of control
over eating during the episode).
 Clinical Presentation
• The binge-eating episodes are required to be associated
with at least three of the following:
• eating more rapidly than normal; eating until feeling
uncomfortably full;
• eating large amounts of food when not physically
hungry;
• eating alone because of embarrassment of how much is
being eaten;
• and feeling disgusted with oneself, depressed, or guilty
after the episode.
• The severity of BED is determined by the number of
binge-eating episodes per week (1-3 = mild; 4-7 =
moderate; 8-13 = severe; 14 or more = extreme).
Desired Outcomes
• Reduce distorted body image
• Restore and maintain healthy body weight
• Establish normal eating patterns
• Improve psychological, psychosocial and physical
problems
• Resolve contributory family problems
• Enhance compliance
• Prevent relapse
• Weight loss (for binge-eating disorder)
Treatment
A. Anorexia Nervosa
1. Non-pharmacologic
• Psychotherapy – best approach (CBT, dialectical
behavorial therapy, family therapy, etc.
• Younger patients – family therapy best first line
treatment
• 6 mos. – I yr therapy
• Interpersonal psychotherapy (interpersonal
relationship and functioning
• CBT (positive reinforcement for weight gain)
• Oral refeeding with liquid formula (most
common approach)
Treatment
• NGT refeeding for those who refuse to eat
• TPN for severely malnourished patients
2. Pharmacologic
• Antidepressants – not indicated for acute
treatment of AN
- used only is depression, anxiety,
obsessions/compulsions after target weight is
obtained
- SSRI are preferred (better tolerated and
safer CVS profile); Fluoxetin is most extensively
studied
Treatment
• Antipsychotics – 1st and 2nd gen drugs
- 2nd gen antipsychotics (wt gain,
reduced depression, anxiety etc)
- 2nd gen risperidone, olanzapine,
quetiapine
• Misc. Agents – metoclopramide(reduce bloating,
early satiety, abdominal pain) short acting B2
alprazolam, lorazepam (reduce anxiety associated
with eating)
• topiramate reduce BMI, binge eating frequency
and body weight
Treatment
• Zonisamide with or without CBT for 16
weeks reduce binge eating; associated with
weight loss (dropout rate is high because of
intolerability)
• Orlistat with caloric restriction resulted to
significant weight loss.
 Evaluation of Therapeutic Outcomes
A. Anorexia Nervosa
Key indicators of response
- reduced frequency and severity of abnormal eating
habits
- normalized exercise patterns
- N lab tests
- sustained weight close to age-matched normal
Daily recordings of food intake, menses, patterns of eating
Weight gain of not more than 0.2 to 0.5 kg/wk ideal
Target weight 90 to 95% of normal or BMI greater than
18.5kg/m2
 Evaluation of Therapeutic Outcomes
B. Bulimia
Comprehensive Assessment
- description of psychiatric symptoms
- physical findings
- frequency and severity of binge-purge episodes
- laxatives and ipecac use
- exercise patterns
- laboratory and ECG abnormalities
- interpersonal and relationship problems should be
evaluated
Response to treatment is 4-8weeks from onset of tx
If TCA is used drug serum concentration determination q 3-
6mos
 Evaluation of Therapeutic Outcomes
B. Bulimia
1. Non pharmacologic
- non drug strategies similar to AN
- CBT strongest evidence of support
- family therapy less effective than in AN
- nutritional counselling, planned meals and self
monitoring (interrupt binge-purge cycle)
2. Pharmacologic
Antidepressants
– used in acute and maintenance phase of BN
- reduce depression, anxiety, obsessions and impulsive
behavior
 Evaluation of Therapeutic Outcomes
B. Bulimia
- response seen in 6-8 weeks use
- SSRIs are preferred; Fluoxetin only FDA approved for
BN
- bupropion is contraindicated in BN
- complete PE, ECG, laboratory work up must be done
prior to drug introduction
- rule out hypokalemia, bradycardia and AV block
 Evaluation of Therapeutic Outcomes
C. Binge-Eating Disorder (BED)
1. Non-pharmacologic
- individual and group CBT universally accepted for
BED
- IPT comparable results with CBT
- weight loss focused programs – most effective in losing
weight, for those who are obese
2. Pharmacologic
-antidepressants as monotherapy
– reduce binge eating, decrease BMI less
depression
- citalopram, esatalopram, fluroxamine,
fluroxetine, sertraline, atomoxetine, venlafaxine
 Evaluation of Therapeutic Outcomes
C. Binge-Eating Disorder (BED)
- lisdexamfetamine (prodrug of
dextroamfetamine)
- mod to severe BED
Eating Disorder Inventory (EDI)
 The EDI is a 64 item, self-report for the
assessment of psychological and behavioral traits
common in anorexia nervosa (AN) and bulimia.
 EDI consists of eight sub-scales measuring: 1)
Drive for Thinness, 2) Bulimia, 3) Body
Dissatisfaction, 4) Ineffectiveness, 5)
Perfectionism, 6) Interpersonal Distrust, 7)
Interoceptive Awareness ,8) Maturity Fears
Anorexia Nervosa: Treatment
Determine inpatient vs. day treatment vs. outpatient
Multidisciplinary teams are ESSENTIAL!
Primary care provider
Psychiatrist
Individual therapist
Family therapist
Nutritionist

1 : weight restoration
st

2 : psychological
nd

3 : maintinance (long-term)
rd
Medical Admission Criteria
<75% ideal body weight
Hypothermia T<36
Bradycardia HR<50 while awake, <45 asleep
Orthostasis-drop in sbp >10, increase in
HR>35
Dehydration
Severe hypokalemia (<2-3 mmol/L) or other
electrolyte abnormality
Acute medical complication
Severe depression/suicidality– Psychiatric
admit
Refractory to outpatient treatment
Anorexia Nervosa: Therapy
Best evidence is for family-based treatment
(Maudsley approach)
Who: younger patients who live at home, intact family
Philosophy: no-blame, family did not cause anorexia; family
is the best resource to help her get better
Elevate family’s anxiety about the gravity of the illness.
Empower parents to do whatever they need to do to get the
anorexic to eat. Align siblings with the patient for support.
Externalize the anorexia.
“Family Meal”
Once weight-restored: explore the family dynamics and
psychological issues.
Anorexia Nervosa: Medications
No approved medication treatments for Anorexia Nervosa

Prozac (or other SSRI) for co-morbid depression or anxiety

Low-dose Atypical Antipsychotics off-label for near-

psychotic thinking that is characteristic of anorexia,
Zyprexa may help with weight gain
- problem: informed consent for risks of weight gain
ANOREXIA NERVOSA
Prognosis:
40% → recover.

30% → continue with milder course.

30% → chronic cases.

Risk of death
 Suicide
Cardiac arrest
Malnutrition

> 3 years of illness: prognosis is poor

Diagnostic Criteria for Bulemia Nervosa DSM-5
A. Recurrent episodes of binge eating:
(1) Eating large amount in a discrete period of time
(2) lack of control over eating
B. Recurrent compensatory behavior in order to
prevent weight gain.
C. Binge eating and inappropriate compensatory
behaviors is at least once a week for 3 months.
Bulemia: Epidemiology
Lifetime Prevalence
1.5% women
0.5% men

Prevalence of binge-purge behaviors:

13% girls
7% boys
Bulemia: Etiology
Family dynamics

Individual
Temperament
(ie. impulsive)

Societal, cultural

Media factors biological

Medical Complication
Electrolyte abnormalities
Dental – loss of enamel, chipped teeth, cavities
Parotid enlargement
Conjunctival hemorrhages
Calluses on dorsal side of hand (Russel’s sign)
Esophagitis
hematemesis
Latxative-dependent: cathartic colon, melena, rectal
prolapse
Bulemia: Treatment
 Multidisciplinary team
Primary care provider
Psychiatrist
Family therapist
Nutritionist
 Evidence based : CBT + Antidepressant (SSRI)
Bulemia: Treatment (Therapy)
Family therapy is a good option if patient is young
and still lives at home (But not as much evidence as
for Anorexia)
Interpersonal therapy (IPT) (short-term treatment
focused on life transitions)
Psychodynamic Psychotherapy (good for long-term
results in people with chronic depressive and
personality symptoms)
Nutrition plan, exercise, physical activity
Bulemia: Medicaions
High-dose Fluoxetine/Prozac (SSRI) – very good
evidence!
Sertraline/Zoloft (SSRI) – some good evidence
Buproprion/Wellbutrin (other antidepressant) –
contraindicated! (risk of seizures if history of
purging)
Topiramate/Topomax (mood stabalizer,
promotes weight loss) – some good evidence, but
use with caution esp if low-weight
Bulemia: Prognosis
33% remit every year
But another 33% relapse into full criteria
Adolescent-onset better prognosis than adult-onset
Death-rate = 1%
Binge Eating Disorder
Binge Eating Disorder- Diagnosis
Also needs 3 of the following:
Eating much more rapidly than normal
Getting uncomfortably full
Large amounts of food when not physically
hungry
Eating alone because embarrassed about how
much one is eating
Feeling disgusted with oneself, depressed, or
guilty when over-eating
DSM-5 Diagnostic Criteria for Binge Eating
Disorder
 Eating, in a discrete period of time , large amount
 Lack of control over eating during the episode
Binge eating occurs, on average, at least once a week
for three month
Binge Eating Disorder:
Epidemiology
Most common eating disorder
Lifetime prevalence:
3.5% women
2% men
Binge Eating Disorder:
Treatment (Medication)
SSRI
high dose reduces binge behavior short-term
but doesn’t help weight loss

Topomax, Zonisamide (anticonvulsants, mild

mood stabalizer)
Helps binge reduction
Helps weight loss
Caution for adverse effects, high discontinuation rates
Binge Eating Disorder:
Treatment (Therapy)
Therapies either prioritize…
Weight loss
Binge-reduction
Neither (ie. relationships, depression etc)

Group psychotherapy
There is little evidence that obese individuals who
binge should receive different therapy than obese
individuals who do not binge