Bulimia dan Anoreksia Nervosa

01Pathophysiology

Anorexia Nervosa

The core psychopathology in anorexia nervosa, as defined in the PPDGJ-III, is a distortion of body image where the patient harbors a persistent, irrational dread of becoming fat. This drives the patient to deliberately reduce and maintain body weight well below a healthy threshold. The weight loss is not passive or accidental; it is actively induced and sustained by the patient through avoidance of calorie-dense foods and one or more compensatory behaviors such as self-induced vomiting, purgative use, excessive exercise, or the use of appetite suppressants and diuretics.

The sustained caloric deficit triggers a cascade of hypothalamic-pituitary-gonadal (HPG) axis suppression. The hypothalamus reduces pulsatile GnRH secretion, leading to low LH and FSH, which in women manifests as amenorrhea and in men as loss of libido and potency. This is a functional, starvation-induced hypogonadism, not a primary gonadal defect. The PPDGJ-III notes one important exception: menstrual bleeding may persist in anorexia patients receiving exogenous hormonal therapy (oral contraceptive pills), so amenorrhea alone is not a reliable screening tool in that population.

Beyond the gonadal axis, chronic starvation leads to elevated cortisol (the body's stress response to energy deprivation), increased growth hormone (a counter-regulatory attempt to mobilize fuel stores), altered peripheral thyroid hormone metabolism (low T3 "euthyroid sick syndrome"), and abnormal insulin secretion. These endocrine derangements explain much of the clinical picture: bradycardia, hypothermia, dry skin, hair loss, and lanugo.

When onset occurs before puberty, the PPDGJ-III highlights that pubertal milestones are delayed or arrested entirely. In girls, breast development stalls and primary amenorrhea occurs. In boys, genital development remains prepubertal. With recovery, puberty resumes, though menarche may be delayed.

Bulimia Nervosa

Bulimia nervosa shares the same underlying psychopathological fear of fatness, but the behavioral pattern is fundamentally different. The PPDGJ-III describes the cardinal feature as a persistent preoccupation with eating accompanied by episodes of irresistible craving (craving) for food. The patient experiences recurrent binge eating episodes, consuming abnormally large quantities of food in a short period while feeling a complete loss of control.

Following the binge, the patient attempts to counteract the expected weight gain through compensatory behaviors: self-induced vomiting, laxative or diuretic abuse, intermittent starvation, or the use of appetite suppressants and thyroid preparations. The PPDGJ-III adds a clinically important note: in patients with diabetes mellitus, the compensatory behavior may take the form of deliberate omission of insulin therapy to prevent caloric assimilation.

The repeated vomiting leads to hypokalemia and metabolic alkalosis (loss of H+ and Cl-), parotid gland hypertrophy from repeated stimulation, and erosion of dental enamel from gastric acid exposure. Laxative abuse instead produces metabolic acidosis with volume depletion.

The PPDGJ-III explicitly notes that a prior episode of anorexia nervosa is often present in the patient's history. The interval between the anorexia episode and bulimia ranges from several months to several years. The prior anorexia episode may have been clinically obvious or may have been "hidden," presenting only as modest weight loss, a transient phase of amenorrhea, or both.

An important distinction the PPDGJ-III makes: bulimia nervosa must be differentiated from depressive disorder, because bulimic patients frequently exhibit comorbid depressive symptoms. The test-writer may present a patient with binge-purge behavior and prominent sadness to see if you correctly identify bulimia as the primary diagnosis rather than depression with eating changes.

02Classification and Clinical Manifestation

PPDGJ-III Classification of Eating Disorders

Clinical Manifestation

03Diagnostic Workup

For anorexia nervosa, the PPDGJ-III requires that the diagnosis not be made casually. The guideline states that for a definite diagnosis, all five criteria (a through e) must be present. The initial step is calculating the BMI. A value of 17.5 or lower is the quantitative threshold established in the guideline. In pre-pubertal patients who have not yet reached their expected growth trajectory, the equivalent criterion is a failure to achieve expected weight gain during the growth period, rather than a percentage loss from a prior baseline.

Next, you must establish that the weight loss is self-induced. The vignette will typically describe dietary restriction of fatty or calorie-dense foods combined with at least one additional behavior (vomiting, purgative use, excessive exercise, or pharmacological suppression of appetite). The critical point is that the weight loss is intentional and maintained by the patient, not due to an organic cause.

Body-image distortion is the psychopathological hallmark. Look for statements in the vignette such as "the patient believes she is overweight despite being underweight" or "expresses intense fear of gaining weight." The PPDGJ-III phrases this as an "overvalued dread of fatness."

The endocrine workup is confirmatory. Expect to see low gonadotropins (LH, FSH), amenorrhea, elevated cortisol, elevated growth hormone, low T3, and abnormal insulin secretion. These findings are secondary to the starvation state and are expected to normalize with weight restoration.

For bulimia nervosa, diagnosis is primarily clinical. The PPDGJ-III requires documentation of (a) persistent food preoccupation with uncontrollable craving and binge episodes, (b) compensatory anti-fattening behaviors, and (c) the characteristic psychopathology of fat-phobia with a self-imposed weight ceiling. Laboratory findings support the diagnosis but do not define it. Hypokalemia is the most high-yield lab abnormality to recognize. An elevated serum amylase (from parotid hypertrophy, not pancreatitis) is a classic clue in a vignette. Blood gas analysis helps distinguish the type of purging: vomiting produces metabolic alkalosis, while laxative abuse produces metabolic acidosis.

The PPDGJ-III makes the important point that a prior episode of anorexia nervosa frequently exists in the history. The test-writer may include this as a timeline detail to help you confirm bulimia over other differentials.

Differential Diagnoses per PPDGJ-III

For bulimia nervosa, the PPDGJ-III explicitly flags depressive disorder as the primary differential, since bulimic patients frequently have comorbid depressive symptoms.

04Management and Treatment

Anorexia Nervosa

Step 1: Assess medical stability. The first priority is determining whether the patient requires inpatient admission. Indications for hospitalization include BMI below 15, heart rate below 40 bpm, systolic blood pressure below 90 mmHg, significant electrolyte disturbances (especially hypokalemia and hypophosphatemia), or active suicidal ideation.

Step 2: Nutritional rehabilitation. Begin refeeding cautiously, typically starting at 1000 to 1200 kcal/day and increasing by 200 kcal every 2 to 3 days. The critical danger during this phase is refeeding syndrome, which results from rapid insulin-mediated cellular uptake of phosphate, potassium, and magnesium when carbohydrate intake resumes after prolonged starvation. Monitor serum phosphate, potassium, and magnesium daily during the first 1 to 2 weeks. Supplement phosphate prophylactically if levels trend downward.

Step 3: Psychotherapy. For adolescent patients, Family-Based Treatment (FBT), also known as the Maudsley approach, is the most evidence-supported intervention. Parents are empowered to take control of the patient's nutrition in Phase 1, then gradually return autonomy to the adolescent as weight is restored. For adults, CBT addressing body-image distortion and maladaptive eating behaviors is the primary approach.

Step 4: Pharmacotherapy. There is no medication proven to induce weight gain in anorexia nervosa. Do not start SSRIs in the acutely malnourished patient, as serotonergic medications are less effective (and potentially more harmful) in the setting of nutritional depletion. Once partial weight restoration has occurred, fluoxetine or other SSRIs may be considered for comorbid anxiety or depressive symptoms, or for relapse prevention.

Step 5: Endocrine monitoring. Expect amenorrhea to resolve with weight restoration. Do not prescribe estrogen replacement solely to restore menses, as this does not address the underlying hypothalamic suppression. Monitor bone density with DEXA in patients with prolonged amenorrhea (greater than 6 to 12 months), as osteoporosis is a significant long-term complication.

Bulimia Nervosa

Step 1: Interrupt the binge-purge cycle. The immediate goal is breaking the behavioral loop. Structured meal planning with regular meals and snacks (typically 3 meals and 2 to 3 snacks daily) reduces the physiological hunger that triggers binges.

Step 2: Correct electrolyte abnormalities. Potassium replacement is often necessary. Oral supplementation (20 to 40 mEq KCl daily) is usually sufficient unless the patient is severely hypokalemic (below 3.0 mEq/L) or symptomatic, in which case intravenous replacement with cardiac monitoring is indicated.

Step 3: CBT. Cognitive-Behavioral Therapy is the first-line treatment for bulimia nervosa and has the strongest evidence base. A standard course involves 16 to 20 sessions over 4 to 5 months. The therapy targets the cognitive distortions around body shape, the behavioral pattern of dietary restriction leading to binge episodes, and the use of compensatory purging.

Step 4: Pharmacotherapy. Fluoxetine at 60 mg/day is the recommended pharmacological agent. This dose is notably higher than the 20 mg/day used for depression. It reduces binge frequency and purging behavior independent of its antidepressant effect. If fluoxetine is not tolerated, other SSRIs may be tried, though evidence is strongest for fluoxetine. Bupropion is contraindicated in bulimia nervosa due to an increased risk of seizures in purging patients.

Step 5: Monitor for complications. Regular dental examinations are important for patients with chronic vomiting. Esophageal tears (Mallory-Weiss) and, rarely, esophageal rupture (Boerhaave syndrome) are life-threatening complications of forceful vomiting.

05Differential Diagnosis and Distractors

06Traps and High-Yield Pearls

The most common way students lose points on eating disorder questions is by confusing the weight criterion. The PPDGJ-III draws a hard line: anorexia nervosa requires the patient to be significantly underweight (BMI $\le 17.5\backslash leq\; 17.5$ or weight 15% below expected). If the vignette describes a patient with binge-purge behavior but a normal BMI, the answer is bulimia nervosa, not anorexia. Many students default to "anorexia" whenever they see vomiting or food restriction, but the weight status is the decisive discriminator.

A second frequent trap involves the endocrine findings. Students may see amenorrhea, elevated cortisol, and low T3 in a vignette and be tempted to pursue an endocrine workup for Cushing syndrome or hypothyroidism. The key is recognizing that these hormonal derangements in the context of severe underweight and deliberate food restriction are secondary to the starvation state, not primary endocrine disease. They resolve with nutritional rehabilitation.

Third, the PPDGJ-III explicitly states that a prior anorexia nervosa episode is commonly part of the history in bulimia patients. If the vignette includes a timeline where the patient was severely underweight years ago and now presents at normal weight with binge-purge behavior, this historical detail confirms bulimia nervosa and should not confuse you into choosing anorexia.

Fourth, watch for the bupropion contraindication. A vignette may describe a bulimic patient with comorbid depression and ask about appropriate pharmacotherapy. Bupropion lowers the seizure threshold and is contraindicated in patients who purge. The correct answer is fluoxetine at 60 mg/day.

Finally, in the PPDGJ-III framework, atypical variants exist for both disorders. If a vignette describes a patient who meets most but not all criteria (e.g., all features of anorexia but menstruation is preserved, or all features of bulimia but binge episodes are infrequent), the correct classification is the atypical form. Do not dismiss the diagnosis entirely just because one criterion is absent; the PPDGJ-III accommodates partial presentations through the atypical categories.

The core competency being tested is your ability to (1) distinguish anorexia from bulimia based on weight and behavioral pattern, (2) recognize that endocrine abnormalities in anorexia are secondary and reversible, and (3) select the correct first-line therapy for each condition (FBT/nutritional rehabilitation for anorexia, CBT plus fluoxetine 60 mg for bulimia).