Psychiatry

A third-grade boy cannot stop moving in the exam room, sliding off his chair onto the floor and then climbing onto his mother's lap; his teacher at school complains that he cannot pay attention and blurts out in class. Across the waiting room sits a seventy-eight-year-old man; his wife says he has become a different person over the past six months — once meticulous and considerate, he now screams at store clerks at the supermarket, insists he has not eaten moments after finishing a meal, and has started taking off his pants in public. One is a developing brain with every door thrown open; the other is a degenerating brain going dark room by room. The two ends of the age spectrum in psychiatry are the pairing the licensing exam loves most to place side by side on the same page.

To understand ADHD, start back at the prefrontal cortex. Its essence is prefrontal executive-function deficiency: dopamine and norepinephrine signaling in the prefrontal cortex runs weak, so the child cannot sustain impulse inhibition or maintain attention. Because it is a developmental problem, the symptoms must be present since childhood and cannot first appear in adulthood; and because it is a whole-brain regulatory problem, it cannot occur in only one setting — it must show up across settings. Finally, an inability to sit still can just be a personality trait; only when it causes social, academic, or occupational impairment does it graduate into a disorder. So behind the three locks lies a single causal chain — just remember before age 12, two settings, functional impairment. The old "before age 7" cutoff is the outdated distractor the exam loves to dangle; symptoms confined to school, or onset in middle school, cannot be diagnosed unless all three locks open together. Medication follows the same mechanism: since prefrontal dopamine is deficient, central stimulants push it up, with methylphenidate and amphetamine-class agents working best; for patients who cannot tolerate stimulants, who have tics, or where abuse potential is a concern, switch to atomoxetine, a norepinephrine reuptake inhibitor, or to α2 agonists such as clonidine and guanfacine. Stimulants may temporarily affect appetite, growth, and sleep onset, but comorbid tics are not an absolute contraindication — that old belief has long since been corrected.

The core of Tourette syndrome is overactivation of the basal ganglia dopamine system and D2 receptor supersensitivity, so the reasoning chain runs straight through: suppress tics with D2 antagonists, and a dopamine agonist only pours fuel on the fire. Haloperidol, pimozide, risperidone, and aripiprazole can all improve tics; clonidine and guanfacine have fewer side effects and are the common first line, particularly suited to children with comorbid ADHD. Its heritability is high — traditional textbooks describe autosomal dominant inheritance with incomplete penetrance, while the modern view leans toward polygenic inheritance, though the exam still expects the old answer when it poses the question this way. One myth needs debunking: not every patient outgrows it naturally; the tics only partially remit. The core of autism spectrum disorder is deficits in social-emotional reciprocity plus restricted, repetitive behaviors, and the exam loves to ask about treatment, because it slips in the option that sounds most reasonable to deceive you. Applied behavior analysis, early intensive behavioral intervention, and speech therapy are all evidence-based; cognitive behavioral therapy is also effective for comorbid anxiety, depression, and OCD, but sensory integration therapy has no high-quality randomized controlled trial support for the core symptoms of autism — this is the most common trap. Conduct disorder is not a pediatric-only diagnosis; past age 18, if criteria are still met but the threshold for antisocial personality disorder has not been reached, it can still be diagnosed, and the two can even coexist — the diagnosis does not automatically switch on someone's birthday.

The most important thing to remember about normal aging is the direction: dopamine, acetylcholine, norepinephrine, and serotonin all decline together, cerebral blood flow and oxygen utilization decline as well, while IQ is better preserved through crystallized intelligence and can remain stable to about age 80. The exam loves to reverse the direction — seeing "norepinephrine rises with normal aging" should be crossed out immediately. Several geriatric figures are also frequently tested: the prevalence of late-life depression is about 15%, arthritis is the most common cause of disability in the elderly rather than dementia, and persecutory delusions are the most common type of late-onset delusional disorder. New-onset psychotic symptoms in the elderly usually respond to low-dose antipsychotics — "poor response" is a reverse trap — but watch for side effects such as extrapyramidal symptoms and falls.

Last comes the differentiation of the dementias. Frontotemporal dementia damages the frontal lobe and anterior temporal lobe, so what collapses first, early on, is personality, behavior, social cognition, and language, while learning and memory are relatively preserved; onset is also earlier, often before age 65. Alzheimer disease damages the medial temporal lobe and hippocampus, so what collapses first, early on, is recent memory, while social cognition is relatively preserved instead. One line to close it out: frontotemporal dementia is the person changed, Alzheimer disease is the facts forgotten. If a question describes FTD's social cognition as preserved early on, that is a reverse trap — it is impaired, not preserved, and getting this direction backward will cost you points across the whole set of linked questions. The entire chapter really comes down to a single habit of mind: first ask whether this brain is heading toward development or decline, then ask which transmitter or which region has gone wrong, and the symptoms will fall into place on their own.

A nineteen-year-old male college student is brought into the emergency department by his family. His grades have been sliding for three months, and he has recently started tearing his room apart looking for a listening device, shouting into empty air at midnight, don't tell me to jump. His mother says he has become completely hollow — he will not bathe, will not speak, his eyes have gone vacant. Auditory hallucinations, delusions, plus flat affect and loss of motivation — three clues lined up side by side, pointing to schizophrenia. To understand this disease, start back at the dopamine pathways. Excess dopamine in the mesolimbic system props up the positive symptoms — hallucinations and delusions; deficient dopamine in the mesocortical pathway flattens affect, extinguishes motivation, and drives the social withdrawal that props up the negative symptoms.

Haloperidol, the representative first-generation antipsychotic, primarily blocks D2 receptors, so it can suppress positive symptoms but is powerless against negative symptoms, and because it blocks dopamine in the nigrostriatal pathway as well, it carries a heavy burden of extrapyramidal side effects. Second-generation drugs block both D2 and 5-HT2A; serotonin's inhibition of striatal dopamine is thereby loosened, so dopamine at the cortical end is somewhat freed up, giving a slightly better effect on negative symptoms and fewer extrapyramidal side effects. The four A's that Bleuler left behind form a mnemonic skeleton from a century ago — loosening of associations, autistic thinking, flattened affect, and ambivalence — and the key to autistic thinking is subjectivity, a self-centered distortion of objective reality; if a question says it emphasizes objectivity, that is a reverse trap. The definitions of hallucination, illusion, and delusion are actually crisp: a hallucination is a perceptual experience arising without any external stimulus, an illusion is a stimulus whose nature is misjudged, and a delusion is a fixed false belief that neither reality nor logic can shake. The most common hallucination in schizophrenia is auditory, with command auditory hallucinations being the most classic and the most dangerous; olfactory hallucinations should instead raise suspicion for temporal lobe epilepsy or another organic cause, because they are actually uncommon in schizophrenia — this is exactly the trap the licensing exam loves to dig.

The diagnostic timeline to remember is six months: symptoms including the active phase must persist for at least six months, counting the prodromal and residual phases as well; one to six months is called schizophreniform disorder, and less than one month is called brief psychotic disorder. The exam loves to misstate six months as one year — cross it out on sight. Haloperidol is first-generation; do not flip this classification. Medication-induced akathisia leaves the patient restless and unable to sit still, pacing back and forth, and is most easily misjudged as agitation, so adding more antipsychotic only makes it worse — the correct management is to reduce the dose or add a β-blocker such as propranolol. Patients who develop extrapyramidal symptoms early are, in the long run, more likely to develop irreversible tardive dyskinesia, which is also why second-generation drugs have an advantage on this point.

Clozapine is the special case in this group: it is the only drug with proven efficacy in treatment-resistant schizophrenia and the only one shown to reduce suicide risk; but the price is the risk of agranulocytosis, so what must be monitored regularly is the white cell count, not the drug level. Because of this risk, it is never first-line but instead the reserve trump card for refractory patients. Other important side effects include a lowered seizure threshold, myocarditis in the first one to two months, decreased bowel motility, sialorrhea, and metabolic syndrome. One line to close it out: clozapine is the most effective but most dangerous drug — to save the sickest patients, you must draw blood the most often.

Prognosis also grows straight out of the mechanism: the more a case resembles affective psychosis, the more optimistic the outlook — acute onset, a precipitating factor, late onset, female, predominantly positive symptoms, and a family history of affective illness are all good prognostic signs; the more it resembles pure schizophrenia, the worse the outlook — insidious onset, no precipitating factor, early onset, male, prominent negative symptoms, and a family history of schizophrenia are all poor prognostic signs. Epidemiology calls for three numbers: prevalence is about one percent and roughly equal between the sexes — "women are affected twice as often as men" is wrong; age of onset runs fifteen to twenty-five years in men, earlier than the twenty to thirty years typical of women; lifetime suicide mortality was written as about ten percent in traditional textbooks, revised by newer meta-analyses to about five percent, but whichever figure is used, it remains far higher than the general population and far below inflated options such as twenty-five to fifty percent. Finally, on the legal side, involuntary hospitalization must follow the procedures of the Mental Health Act, requiring a severely ill patient, a risk of harm to self or others, plus a review mechanism — it is never one physician's call alone.

Three women take a seat in the clinic, one after another: a thirty-five-year-old new mother crying day and night, feeling useless, often lying awake until dawn; a twenty-six-year-old woman who falls apart emotionally and throws things every week before her period, with symptoms vanishing the moment her period starts; a twenty-two-year-old college student who, three weeks after a car accident, has recurrent nightmares, jumps at the sound of a car horn, and avoids every situation involving driving. Three stories — depression, premenstrual dysphoria, and posttraumatic stress — yet underneath lies the same single throughline: the tug-of-war between the monoamines and the amygdala.

The most classic model of major depressive disorder is monoaminergic hypofunction. Norepinephrine comes from the locus coeruleus, serotonin from the raphe nuclei, and dopamine from the ventral tegmental area and substantia nigra — do not swap these nuclei, since the licensing exam loves to exchange the sources of norepinephrine and serotonin. Declining function produces depression, and the action of antidepressants is to inhibit reuptake so that monoamines accumulate in the synapse — note that it is inhibition, not enhancement, and this direction accounts for the bulk of the reverse traps. All three transmitters are related to depression, and remembering only one of them is also a common mistake. Imaging and sleep are simply extensions of this same chain: in depression, metabolism decreases in the anterior brain, especially the left dorsolateral prefrontal cortex, with mania showing the reverse; sleep shows shortened REM latency, entering REM sooner after falling asleep, not later — this direction is also frequently written backward. The first episode of bipolar disorder can be either a depressive episode or a manic episode, and is not necessarily manic — this is a classic distractor; long-term patients may develop cognitive decline, and those with a family history of schizophrenia also carry a higher risk of developing the disorder, because psychotic disorders cluster within families.

The teratogenicity of mood stabilizers in pregnancy is easy to remember by following the direction of the organ affected: lithium harms the heart, causing Ebstein anomaly with downward displacement of the tricuspid valve; valproate and carbamazepine harm the spine, causing neural tube defects; the older literature on lamotrigine once reported a signal for cleft lip and palate, but newer large-scale meta-analyses show an absolute excess risk below one in five hundred fifty, no longer considered significant, so the drug most to be avoided in pregnancy is actually valproate, while lamotrigine is instead one of the relatively safest options. Both premenstrual syndrome and premenstrual dysphoric disorder occur during the luteal phase, when estrogen and progesterone are both still present, so hot flashes are never among the symptoms — hot flashes only occur with the estrogen deficiency of menopause; delusions are a psychotic symptom requiring a separate diagnosis and fall outside the scope of premenstrual dysphoric disorder — these two "does not belong" options are exactly the distractors the exam loves to insert.

Suicide risk assessment has one direction you must never reverse: psychosis is a high-risk factor, not a protective one, especially when command auditory hallucinations demand suicide; the protective factors are family relationships, social support, and religious deterrents. Every disorder on the anxiety spectrum is at its core amygdala hyperarousal combined with insufficient prefrontal inhibition — the only differences are what is feared and for how long. Generalized anxiety disorder requires six months of symptoms plus three somatic symptoms, peaks in onset during the twenties and thirties, and becomes chronic in about sixty percent of cases — it is not a mild anxiety that resolves easily. The mechanism of panic disorder is a burst of norepinephrine from the locus coeruleus plus a hypersensitive brainstem false-suffocation alarm, which is why patients become convinced they are having a heart attack and panic disorder is the anxiety disorder most likely to send someone rushing to the emergency department; the diagnosis requires an attack peaking within minutes plus at least one month of fearing recurrence or a resulting behavior change. The circuit in obsessive-compulsive disorder is overactivation of the cortico-striato-thalamo-cortical loop plus serotonergic dysregulation — obsessions raise anxiety, compulsions lower it, and the cycle then reinforces itself. The two post-trauma stages are the same illness divided by the one-month mark: before one month it is called acute stress disorder, and past one month it is upgraded to posttraumatic stress disorder; the criteria for acute stress disorder explicitly include a cluster of dissociative symptoms — amnesia, derealization, and depersonalization — so if a question states that acute stress disorder does not include dissociation, that is wrong.

In terms of medication, first line across the entire spectrum is a serotonin reuptake inhibitor or a serotonin-norepinephrine reuptake inhibitor plus cognitive behavioral therapy — that is the backbone. Each disorder has its own small differences: obsessive-compulsive disorder needs higher doses and takes longer to show benefit, with exposure and response prevention as its core treatment, and treatment-resistant cases can add clomipramine, a potent serotonergic tricyclic antidepressant, or augment with a low-dose antipsychotic. The biggest trap in posttraumatic stress disorder is benzodiazepines — they are not recommended for this disorder, being ineffective while increasing dependence and worsening the long-term course; nightmares and hyperarousal should instead be treated with prazosin, an α1 antagonist; the drugs of choice are serotonin reuptake inhibitors, and the first-line psychotherapies are trauma-focused cognitive behavioral therapy or eye movement desensitization and reprocessing. In panic disorder, short-term benzodiazepines may be used acutely, while the long-term approach is likewise a serotonergic drug plus cognitive behavioral therapy including exposure. Sex distribution and comorbidity are also worth noting: obsessive-compulsive disorder is roughly equal between the sexes with earlier onset in men, the reverse of most other anxiety disorders, which are more common in women; functional gastrointestinal disorders, especially irritable bowel syndrome, are the most common comorbidity with anxiety disorders, with a comorbidity rate of forty to sixty percent, because the two share autonomic hypersensitivity and gut-brain axis dysregulation.

Two beds in the emergency department: in one, a fifty-five-year-old man with alcohol use disorder, three days into abstinence, suddenly trembling, seeing nonexistent insects crawling up the wall, heart rate at one hundred forty, blood pressure one hundred eighty; in the other, a twenty-three-year-old woman taking a serotonin reuptake inhibitor who added the painkiller tramadol on her own, and two hours ago began shaking all over, with myoclonus, a temperature of forty degrees Celsius, and hyperreflexia. Both patients are febrile, agitated, and racing on autonomic overdrive, but in one the brakes have failed and in the other the gas pedal is stuck — and the drugs required are entirely different.

Almost every substance-use question can be cracked with a single principle: the symptoms of intoxication and withdrawal run in opposite directions. With chronic use, a depressant keeps the brakes pressed and the brain enlarges its own gas pedal to compensate; once the drug stops, the brake releases and only a fully open gas pedal is left, so withdrawal brings over-excitation, seizures, and an autonomic storm — this is the fundamental reason alcohol and benzodiazepine withdrawal can be fatal while stimulant withdrawal rarely is. The alcohol withdrawal timeline must be memorized: six to eight hours brings the earliest tremor plus autonomic hyperactivity, twelve to twenty-four hours brings alcoholic hallucinosis with a clear sensorium, twenty-four to forty-eight hours brings generalized withdrawal seizures, and forty-eight to seventy-two hours brings delirium tremens, which carries the highest mortality. The iron rule of treatment is that a benzodiazepine is first-line, because it shows cross-tolerance with alcohol, restores the brake, and prevents seizures and delirium tremens; phenobarbital has a narrow safety window and is not first-line. Vitamin B1 must always be given before glucose — giving glucose first depletes B1 and can precipitate the ophthalmoplegia-ataxia-confusion triad of Wernicke encephalopathy, and magnesium often needs replacing too. The essence of a blackout is inhibition of hippocampal NMDA receptors, so short-term memories cannot consolidate into long-term ones — it is anterograde transient amnesia, not retrograde, with long-term memory preserved and the person's outward behavior possibly looking normal at the time.

On the stimulant side, intoxication with amphetamine, methamphetamine, or cocaine brings agitation, paranoia, auditory hallucinations, and cardiovascular events, while withdrawal is the reverse — fatigue, hypersomnia, depression; management of the acute psychosis is to stop the drug plus give the short-acting antipsychotic haloperidol, and carbamazepine is not used because it has no established indication for amphetamine-induced psychosis. Ketamine is an NMDA receptor antagonist that produces dissociative anesthesia, hallucinations, and memory impairment, and at low doses it has shown rapid onset of benefit in studies of treatment-resistant depression; opioids act through μ-receptor agonism, and the intoxication triad is pinpoint pupils plus respiratory depression plus decreased consciousness, reversed with naloxone, with withdrawal being miserable but rarely fatal. Caffeine withdrawal appears twelve to twenty-four hours after stopping, is dominated by headache plus fatigue, and includes no hallucinations or delusions — describing it as appearing after a week, or as including hallucinations, is always wrong.

The logic of formulation in psychiatric drugs likewise follows the mechanism: acute management needs fast onset, titratability, and monitorability, so the choice is a short-acting drug well absorbed orally or intramuscularly; a long-acting depot injection has a slow onset and cannot be titrated, so it is for maintenance treatment, not acute care. Diazepam is highly lipophilic, so its intramuscular absorption is erratic with poor bioavailability, which is why lorazepam IM, not diazepam IM, is chosen for acute intramuscular injection. Delirium in general has short-acting oral haloperidol as first-line, plus finding the underlying cause, but alcohol and benzodiazepine withdrawal delirium is the exception — a benzodiazepine, not haloperidol, is first-line, because the brake needs restoring to prevent seizures. Three safety warnings: olanzapine IM must not be combined with a parenteral benzodiazepine, since there have been reports of fatal cardiorespiratory depression; haloperidol, especially given intravenously, prolongs the QT interval; and droperidol carries a black-box warning for QT prolongation.

Which drugs need monitoring also should not be reversed: lithium, valproate, and carbamazepine are monitored by checking the serum level, because their therapeutic window is narrow and the risk of toxicity is high; clozapine is monitored by checking the white cell count or absolute neutrophil count, because of the fear of agranulocytosis, not by checking its serum level. The long-term side effects of lithium include nephrogenic diabetes insipidus, hypothyroidism, weight gain, tremor, and teratogenicity in the form of Ebstein anomaly; the precipitants of toxicity are all things that cause lithium retention — dehydration, NSAIDs, thiazide diuretics, ACE inhibitors, a low-sodium diet — and severe toxicity is cleared by hemodialysis. The side effects of serotonin reuptake inhibitors include nausea, sexual dysfunction, insomnia or hypersomnia, weight change, a bleeding tendency, early agitation, hyponatremia in the elderly, and discontinuation syndrome, but a rapid rise in blood glucose is not one of its side effects — that is a reverse trap; discontinuation syndrome is most common with the short-half-life paroxetine and least likely with the long-half-life fluoxetine.

The four types of extrapyramidal symptoms are not arranged at random — onset timing is the axis of management. Acute dystonia appears within hours to days as oculogyric crisis, torticollis, and laryngospasm, treated with the anticholinergic benztropine or diphenhydramine for fast relief; akathisia appears days to weeks later as subjective restlessness and pacing, most easily misjudged as agitation and treated by increasing the dose, which only makes it worse — the correct approach is to reduce the dose or add propranolol; parkinsonism appears weeks to months later as rigidity, resting tremor, and bradykinesia, treated with an anticholinergic or dose reduction; tardive dyskinesia appears months to years later as involuntary orofacial movements that are often irreversible, managed by stopping or switching to an atypical agent and using the VMAT2 inhibitor valbenazine — note that anticholinergics instead worsen it, since those belong to acute dystonia, so do not confuse the two.

Last is the differentiation of those two emergency-department beds. Neuroleptic malignant syndrome is caused by dopamine blockade from antipsychotics: dopamine plunges off a cliff, disabling hypothalamic thermoregulation and producing striatal rigidity, so onset is slow, over days, and the hallmark is lead-pipe rigidity plus decreased reflexes plus elevated CK; the specific antidote is dantrolene to relax the muscles, plus bromocriptine to replenish dopamine. Serotonin syndrome is caused by combining serotonergic drugs — an SSRI, an SNRI, an MAOI, tramadol, linezolid, and the like — so that synaptic 5-HT surges to excess, producing autonomic hyperactivity and neuromuscular overexcitation; onset is therefore fast, over hours, and the hallmark is myoclonus plus hyperreflexia plus tremor, especially in the lower limbs, with cyproheptadine, an antiserotonergic agent, as the specific antidote. Management common to both is to stop the drug, cool the patient, provide supportive care, and give fluids; the difference lies in the antidote. The key distinguishing question is really whether the muscles are rigid or shaking — rigid is neuroleptic malignant syndrome, shaking is serotonin syndrome.

Four patients lie side by side on the ward: a thirty-year-old woman with glove-and-stocking numbness and reduced muscle strength that fails to match any nerve distribution on every test; a twenty-two-year-old woman with a body mass index of fourteen, a heart rate of thirty-eight, a temperature of thirty-five degrees, and no period for six months; a twenty-eight-year-old woman who repeatedly self-harms, one moment treating the head nurse as a god and the next as garbage, chronically empty inside; and in the next bed, a terminally ill patient, fully lucid, insisting on refusing dialysis, while the family wants him forced to continue. Conversion disorder, anorexia nervosa, borderline personality disorder, and end-of-life ethics — this chapter is devoted entirely to these borderlands of the mind.

What the somatic symptom group shares is somatic discomfort plus excessive thoughts, feelings, or behaviors about the symptoms. There is one major DSM-5 change to remember: somatic symptom disorder no longer requires that symptoms be medically unexplained — even when the patient genuinely has coronary artery disease, the diagnosis can still be made as long as the response to the symptoms is excessive and disproportionate; defining it as no cause found on workup is outdated older thinking. To cut cleanly through this group, use two axes: whether the symptom is deliberately produced, and whether there is a tangible external benefit. Not deliberate is conversion disorder or somatic symptom disorder, where the patient's suffering is genuine; deliberate but only to occupy the patient role is factitious disorder; deliberate with an external benefit, such as evading duty or insurance fraud, is malingering, which is not a mental disorder. The core of conversion disorder is that psychological stress is converted into a neurological functional symptom, yet the findings are internally inconsistent with neuroanatomy — glove-and-stocking numbness is the classic example; the most common symptom is limb weakness or paralysis, followed by gait abnormality and psychogenic non-epileptic seizures, which can coexist with true epilepsy, so the episodes cannot be used to rule out true epilepsy. Responding to suggestion, hypnosis, or lorazepam supports the diagnosis rather than being grounds for ruling it out, and this direction accounts for the bulk of the reverse traps; indifference toward a serious symptom can be seen in conversion disorder but is neither specific nor required. The therapeutic attitude is to build trust, acknowledge that the symptom is genuinely real, provide cognitive behavioral therapy plus rehabilitation, and address the underlying stressor; the cardinal sin is telling the patient outright that this is something they have imagined, which destroys the relationship and accomplishes nothing, because to the patient the symptom is real and not deliberately produced.

Body dysmorphic disorder belongs to the obsessive-compulsive-related disorder spectrum, with first-line treatment being a serotonin reuptake inhibitor plus cognitive behavioral therapy; cosmetic surgery and procedures are ineffective and can even be harmful — fixing one flaw simply shifts the attention to the next, and the demands only grow, never shrink. Dissociative disorders involve a disconnection in the continuity of consciousness, memory, identity, or perception, most often related to trauma; DSM-5 has downgraded dissociative fugue to a "with fugue" specifier under dissociative amnesia, dissociative identity disorder consists of two or more personalities alternating with amnesia, and a person with depersonalization feels that they themselves or the world is unreal, yet reality testing remains intact. Confabulation is not dissociation but a manifestation of a memory disorder — the patient fills gaps with fabricated content without any intent to deceive, classically seen in Korsakoff syndrome, that is, B1 deficiency most often seen in chronic alcohol use; do not confuse this classification. The psychiatric complication least likely after organ transplantation is delusional disorder, while the high-risk conditions are adjustment disorder, major depression, posttraumatic stress disorder — especially ICU-related — and delirium.

The core of every eating disorder is that self-evaluation is held hostage by body shape and weight. Anorexia is defined by significantly low body weight, bulimia by compensatory behavior combined with self-evaluation unduly influenced by weight; there are two important DSM-5 changes to remember — anorexia has removed amenorrhea as a required diagnostic criterion, and it no longer mandates a fixed BMI cutoff, replacing it with significantly low body weight relative to what the person needs; a person who has reached significantly low body weight is still diagnosed with the binge-eating/purging type of anorexia even with binge eating or purging present, not with bulimia. The physiologic complications of anorexia are all compensations for chronic malnutrition plus low body fat: low body fat and a falling metabolic rate cause hypothermia, rising vagal tone causes bradycardia and hypotension, falling hypothalamic GnRH causes the hypogonadotropic hypoestrogenism behind amenorrhea, low estrogen plus malnutrition causes osteoporosis, the skin grows lanugo to conserve heat, and vomiting or laxatives cause hypokalemia and metabolic alkalosis — it is hypokalemia, not hyperkalemia. Indications for hospitalization are a weight roughly below seventy percent of ideal body weight, severe arrhythmia or electrolyte abnormality, unstable vital signs, or acute food refusal with suicide risk, with admission chosen according to the complications — psychiatry or internal medicine/pediatrics — rather than automatically pediatrics. Refeeding syndrome follows rapid refeeding, when a surge of insulin drives phosphate, potassium, and magnesium into cells and causes arrhythmia and heart failure, so calories must be increased slowly with phosphate repletion. Weight regain after bariatric surgery is multifactorial, and replacing B12 and iron only addresses the nutritional deficiencies of postoperative malabsorption — it cannot prevent weight regain. First-line treatment for bulimia is fluoxetine at sixty milligrams a day, higher than the antidepressant dose; bupropion is contraindicated in both anorexia and bulimia because of seizure risk.

Personality disorders divide into three clusters: Cluster A, odd/eccentric — Weird — includes paranoid, schizoid, and schizotypal; Cluster B, dramatic/emotional — Wild — includes antisocial, borderline, histrionic, and narcissistic; Cluster C, anxious — Worried — includes avoidant, dependent, and obsessive-compulsive personality disorder. The picture of borderline personality disorder is extreme emotional instability, chronic emptiness, an intense fear of abandonment, recurrent self-harm and suicidal threats, brief dissociation or quasi-psychotic symptoms under stress, and interpersonal relationships swinging between idealization and devaluation. First-line treatment is dialectical behavior therapy, the psychotherapy with the strongest evidence base; psychotherapy plus medication has a synergistic effect; benzodiazepines are ineffective for the core symptoms and carry a risk of dependence and disinhibition, so they cannot be the mainstay. The exam loves to mistake borderline for dependent personality disorder, or to make a benzodiazepine the first choice — both should be crossed out. Questions defining the defense mechanisms love to dig pits: fantasy is drawing comfort from imagined relationships, dissociation is a loss of identity coherence after intense stress, isolation of affect is describing an event in detail while severing the emotion, recounted in a flat tone, projection is attributing one's own unacceptable motives to others to escape responsibility, reaction formation is masking an impulse with the opposite behavior, and sublimation, redirecting an impulse into a socially acceptable channel, is the representative mature mechanism. Kleptomania is at its core impulsive: tension rises before the theft, relief follows the act, and the stolen items are usually not needed and the person could afford to buy them; the difference from ordinary theft lies in planning and motive — ordinary theft is planned and for the value of the object — so saying kleptomania is carefully premeditated is a reverse trap. The A1 criterion for gender dysphoria in children is a strong desire to be of another gender; children, adolescents, and adults alike require symptoms to persist for at least six months, not adults only; a disorder of sex development does not need to be excluded and can be noted as a specifier; the APA explicitly opposes conversion or reparative therapy and calls for affirmative care instead.

Last is ethics. The four principles are autonomy, beneficence, non-maleficence, and justice; most ethics questions are at their core a conflict between two of these principles — locate the conflict first, then weigh it. For a patient with decision-making capacity, the principle of autonomy usually wins out, unless a third party is endangered. The three requirements for a valid autonomous decision are capacity plus adequate disclosure plus voluntariness; the terminally ill patient with normal consciousness and cognition who repeatedly and consistently refuses dialysis should, under the principle of autonomy, have his decision respected, with no need for a court or legal representative to intervene — this is a gift question, yet also one of the most commonly missed. Situations in which informed consent may be waived or modified are: presumed consent in an emergency, a surrogate deciding by the patient's best interest when capacity is absent, the patient voluntarily waiving disclosure with documentation, and the rare case of therapeutic privilege, whose bar is very high and must not be abused. The duty of confidentiality is not absolute and may be broken when there is serious, imminent harm to an identifiable third party, drawing on the spirit of the Tarasoff duty to protect; in the scenario of a patient with HIV who refuses to inform a sexual partner and the partner is already pregnant, first urging the patient to disclose voluntarily is the reasonable first step, and if the patient still refuses, the physician may then disclose — that is the most appropriate approach; merely reminding the patient to disclose falls short, and fully releasing the patient's personal information violates the principle of proportionality. The classification of euthanasia turns on whether the physician actively did something that caused death or simply stopped providing life support: active euthanasia, actively administering a lethal means, is illegal in most jurisdictions; passive euthanasia, withdrawing or withholding life support, is more widely accepted; physician-assisted suicide sits between the two; the doctrine of double effect, giving a sufficient dose of morphine to relieve suffering where hastening death is foreseen but not intended, is ethically acceptable; withdrawing and withholding are ethically and legally equivalent, and misclassifying actively assisting death as passive euthanasia is the most inappropriate description. Genetic testing is mostly a risk assessment rather than an accurate prediction; organ donation must respect the donor's wishes plus honest disclosure, the family must never be deceived, and having a twelve-year-old minor sister donate a kidney raises child-protection ethics concerns and is not permitted.