NUR 175 · Mental Health · one framework

Mental Health Maps

The same five questions, asked about every disorder. Answer them from memory first, then open the card and check.

1 · What is happeningThe change · why the signs follow
2 · How do you knowAssessment · labs · deterioration
3 · How do you fix itPriorities · meds · orders
4 · Who is involvedThe team · delegation
5 · Worse or preventedComplications · teaching

Skim mode: showing only the hook, the highlighted phrase, the never-do rules and the takeaway from each card. Tap Leave skim for the full version.

🧠 Schizophrenia

One-line hook: this is a break with reality that lasts — not a mood problem with psychotic trim (bipolar) and not a sudden confusion from a medical cause (delirium). Psychosis is present even when mood is normal.

1 · What is happening in the body?
  • Too much dopamine in the mesolimbic pathway → the positive symptoms (hallucinations, delusions). This is exactly why dopamine-blocking drugs quiet them.
  • Too little dopamine in the mesocortical pathway → the negative symptoms (flat affect, no drive). Blocking dopamine does not fix these, which is why negative symptoms linger on medication.
  • Blocking dopamine in the nigrostriatal pathway causes EPS; blocking it in the tuberoinfundibular pathway raises prolactin. Every antipsychotic side effect is a pathway you did not mean to hit.
  • Glutamate/NMDA underactivity and loss of grey matter also contribute — this is a brain-structure illness, not a character flaw.
  • Onset is late teens to mid-20s in men, 20s to 30s in women, usually after a vague prodromal phase of withdrawal and odd beliefs.
  • Diagnosis requires 6 months of disturbance with at least 1 month of active symptoms. 1–6 months = schizophreniform; under 1 month = brief psychotic disorder.
2 · How do you know?
  • Positive symptoms = added on: hallucinations (auditory is the most common), delusions (persecutory, grandiose, referential, somatic), disorganized speech (loose associations, word salad, neologisms, clang, echolalia), bizarre or catatonic behavior.
  • Negative symptoms = taken away — the 5 A's: Affect flat, Alogia (poverty of speech), Anhedonia, Avolition (no goal-directed drive), Asociality. These predict long-term disability more than hallucinations do.
  • Cognitive symptoms: poor working memory, impaired executive function, inability to follow multi-step directions. Plan teaching around this.
  • Always ask what the voices are saying — command hallucinations telling the patient to harm self or others are a safety emergency, not just a symptom to document.
  • 📈 Deterioration: stopping medication, new command hallucinations, escalating pacing/clenched fists/loud speech, refusing food or fluids because of poisoning delusions, or a shift from talking about violence to naming a target.
  • 🚨 Rule out first: delirium, substance intoxication/withdrawal, and medical causes. New psychosis in an older adult is delirium until proven otherwise.
3 · How do you fix it?
  • Safety first, then reality. Do not argue with a delusion and do not agree with it. Say what you observe: "I don't hear the voices, but I can see they frighten you. I'll stay with you." Respond to the feeling, not the content.
  • 💊 First-generation (typical) — haloperidol, fluphenazine, chlorpromazine. Strong on positive symptoms, high EPS. 💊 Second-generation (atypical) — risperidone, olanzapine, quetiapine, aripiprazole, ziprasidone. Less EPS, metabolic syndrome instead (weight gain, hyperglycemia, dyslipidemia — check weight, A1C, lipids).
  • 💊 Drug-specific traps: risperidone → hyperprolactinemia (galactorrhea, gynecomastia, amenorrhea); ziprasidone → QT prolongation, get an ECG; olanzapine → the most weight gain; long-acting injectables (haloperidol decanoate, paliperidone) are the answer for nonadherence.
  • 💊 Clozapine — agranulocytosis. Reserved for treatment-resistant disease and it is the only one that lowers suicide risk. ANC monitoring: weekly × 6 months → every 2 weeks × 6 months → monthly under a REMS program. Hold and notify for ANC under 1,000/mm³. Teach: report fever, sore throat, or flu-like symptoms immediately. Also causes myocarditis, seizures at high doses, severe orthostasis, and drooling.
  • ⏱️ Timeline: agitation calms in days, positive symptoms improve over 1–2 weeks and fully by 4–6 weeks, negative symptoms take months. Teach this or she stops the drug at week two.
  • 🚨 Seclusion & restraint — the legal rules (heavily tested): least restrictive intervention first (verbal de-escalation, offer PRN medication, reduce stimuli, time out); requires a provider order; a nurse may initiate in an emergency but must get the order right away; face-to-face evaluation by the provider within 1 hour; order limits 4 hours adult, 2 hours ages 9–17, 1 hour under 9, renewed each period. Monitoring: continuous observation, behavior and circulation/skin checks every 15 minutes, and food, fluids, toileting, and range of motion every 2 hours. Release at the earliest safe moment and debrief. Never write or accept a PRN or "as needed" restraint order, never use restraint for staff convenience or punishment, and never leave a restrained or secluded patient unobserved.
4 · Who is involved?
  • Psychiatrist / psychiatric NP — diagnosis, medication selection, clozapine REMS enrollment, restraint orders and the 1-hour face-to-face.
  • Psychiatric nurse — the constant. Safety checks, mental status, medication administration and cheeking checks, AIMS screening, de-escalation, and the therapeutic relationship that keeps the patient engaged.
  • Pharmacist — ANC tracking, QT and metabolic monitoring, drug interactions, LAI conversion.
  • Social worker / case manager — housing, disability benefits, assertive community treatment, transportation to the clinic. Nonadherence is usually a logistics problem, not a motivation problem.
  • Therapist — CBT for psychosis, social skills training, cognitive remediation.
  • Family — psychoeducation reduces relapse measurably; high expressed emotion (criticism, hostility, over-involvement) at home predicts relapse.
5 · How can it get worse / be prevented?
  • 🚨 Neuroleptic malignant syndrome (NMS) — the antipsychotic emergency. FEVER: Fever (over 103°F), Encephalopathy/altered LOC, Vitals unstable (autonomic instability), Elevated CK and WBC, Rigidity — classically lead-pipe rigidity. Onset is slow, days to weeks after starting or increasing the drug. Stop the antipsychotic, cool, hydrate aggressively, give dantrolene and/or bromocriptine. Mortality is real; myoglobinuria causes renal failure.
  • ⭐ NMS vs serotonin syndrome — the distinction: NMS = dopamine blocked, slow onset (days), lead-pipe rigidity, normal or decreased reflexes, no diarrhea, treated with dantrolene/bromocriptine. Serotonin syndrome = too much serotonin, fast onset (hours), hyperreflexia and clonus (especially lower legs), diarrhea, tremor and agitation, treated with cyproheptadine. Rigid and slow = NMS · Clonic and fast = serotonin syndrome
  • 🚨 The four EPS, in order of when they appear:
    • 1. Acute dystonia — hours to days. Sudden sustained muscle spasm: torticollis (twisted neck), oculogyric crisis (eyes locked upward), opisthotonos (arched back), laryngospasm. This is an emergency — give IM/IV benztropine or diphenhydramine now.
    • 2. Akathisia — days to weeks. Unbearable inner restlessness, pacing, cannot sit still. Constantly mistaken for worsening anxiety or agitation — the wrong move is to increase the antipsychotic. Treat with propranolol, a benzodiazepine, or a dose reduction. Linked to suicide risk.
    • 3. Pseudoparkinsonism — weeks to months. Mask-like face, shuffling gait, cogwheel rigidity, pill-rolling tremor, bradykinesia, drooling. Treat with benztropine, trihexyphenidyl, or amantadine.
    • 4. Tardive dyskinesia — months to years, often permanent. Involuntary lip smacking, tongue protrusion and rolling, chewing, facial grimacing, writhing limbs. Screen with the AIMS scale routinely. Treat with valbenazine or deutetrabenazine (VMAT2 inhibitors) and by changing the antipsychotic. Never treat tardive dyskinesia with benztropine or another anticholinergic — it makes TD worse. Anticholinergics fix the first three EPS, not the fourth.
  • ⚠️ Other complications: anticholinergic effects (dry mouth, constipation → paralytic ileus, urinary retention, blurred vision), orthostatic hypotension (rise slowly), photosensitivity (sunscreen, especially chlorpromazine), lowered seizure threshold, agranulocytosis with clozapine, and polydipsia with water intoxication.
  • 💀 Life expectancy is shortened by roughly 15–20 years, mostly from cardiovascular disease, smoking, and suicide — screen for all three. About 5–10% die by suicide.
  • ✅ Teach patient and family: take the medication even when you feel well, do not stop abruptly, avoid alcohol and street drugs, report fever/sore throat (clozapine) and any new stiffness or high fever (NMS), use sunscreen, rise slowly, and know the relapse signs — sleep changes and withdrawal come before the voices return.
⭐ If you only remember one thing: Do not argue with the delusion — validate the feeling, present reality once, and always ask what the voices are telling them to do. Fever + lead-pipe rigidity = NMS, stop the drug. Clozapine means ANC monitoring and "call for a sore throat."

🎢 Bipolar Disorder

One-line hook: the defining event is mania, not depression — one true manic episode makes it bipolar I forever, no matter how many depressive episodes came first. An antidepressant given alone can be what flips them into mania.

1 · What is happening in the body?
  • Dysregulated norepinephrine and dopamine signaling — too much during mania, too little during depression. The brain's mood thermostat swings instead of holding.
  • Strong genetic loading — the highest heritability of the major psychiatric illnesses. A first-degree relative with bipolar is the single biggest risk factor.
  • Circadian disruption is both a trigger and a symptom — lost sleep can precipitate a manic episode, and mania then destroys sleep further, which is why sleep is a treatment target, not just a complaint.
  • Kindling: each untreated episode makes the next one arrive sooner and easier. This is the argument for lifelong maintenance therapy.
  • Bipolar I = at least one manic episode (≥ 1 week, or any duration requiring hospitalization). Bipolar II = hypomania (≥ 4 days, no psychosis, no hospitalization) plus major depression, never full mania. Cyclothymia = 2+ years of subthreshold swings.
  • Mania with psychosis is common; the psychosis rides with the mood and disappears when the mood normalizes — that is how it differs from schizophrenia.
2 · How do you know?
  • Mania — DIG FAST: Distractibility · Indiscretion (spending sprees, hypersexuality, risky choices) · Grandiosity · Flight of ideas · Activity increase / agitation · Sleep decreased without feeling tired · Talkativeness (pressured speech).
  • Look at the body, not just the mood: not eating, not sleeping, not sitting down, dehydration, weight loss, exhaustion. A patient in acute mania can die of physical exhaustion and dehydration — that is the actual physiologic priority.
  • Behavior on the unit: intrusive, boundary-less, hilarious then instantly enraged, manipulative, splitting staff, provoking other patients, wearing bright disorganized clothing and heavy makeup.
  • Depressive phase looks like MDD but with more hypersomnia, more psychomotor slowing, and higher suicide risk — most bipolar patients spend more total time depressed than manic.
  • 🧪 Screening: Mood Disorder Questionnaire (MDQ); Young Mania Rating Scale for severity. Always ask a depressed patient "has there ever been a period when you needed much less sleep and felt unstoppable?" before starting an antidepressant.
  • 📈 Deterioration: sleep drops to 2–3 hours, speech becomes impossible to interrupt, spending or sexual risk escalates, and mood turns from euphoric to irritable and hostile — irritable mania is the more dangerous mania.
3 · How do you fix it?
  • Acute mania priorities, in order: safety → physiologic needs (fluids, calories, sleep, rest) → decrease stimulation → medication → limits.
  • 🍎 Nutrition trick: they cannot sit for a meal, so give high-calorie, high-protein finger foods and fluids they can carry — sandwiches, burritos, protein shakes, cheese sticks. Weigh daily and record intake and output.
  • 🔇 Environment: private room away from the noise of the unit, dim light, low stimulation, consistent staff. Offer solitary non-competitive physical outlets (walking with staff, writing, exercise bike). Never place an acutely manic patient in group activities, competitive games, or ping-pong tournaments — competition and stimulation escalate mania.
  • Limit setting: short, firm, calm, consistent, and identical from every staff member. State the expectation and the consequence once, then disengage. Do not argue, debate, joke back, or take the insults personally — arguing is stimulation.
  • 💊 Lithium — the mood stabilizer they will test you on. Therapeutic level 0.6–1.2 mEq/L maintenance (up to 1.5 for acute mania). Toxicity above 1.5. Draw the level 12 hours after the last dose, check every few days when starting, then every 1–3 months. Takes 7–14 days to work — cover the gap with an antipsychotic or benzodiazepine. Baselines: renal function, TSH, ECG, pregnancy test (lithium causes Ebstein anomaly).
  • 💊 Lithium sodium and fluid rules — the whole test question: lithium is handled by the kidney exactly like sodium. If sodium or water goes down, lithium goes up. So: drink 2–3 liters of fluid daily, keep sodium intake steady (no sudden low-salt diet, no crash dieting), take with food, and hold and call for vomiting, diarrhea, fever, heavy sweating, or exercise in the heat. Level-raising drugs: thiazide diuretics, NSAIDs, ACE inhibitors, ARBs — use acetaminophen instead of ibuprofen.
  • 💊 Other stabilizers: valproate/divalproex (level 50–125 mcg/mL; monitor LFTs, ammonia, platelets; neural tube defects — a pregnancy test before starting); carbamazepine (agranulocytosis, hyponatremia, Stevens-Johnson — screen for HLA-B*1502 in patients of Asian ancestry; autoinduces its own metabolism); lamotrigine (best for the depressed pole — titrate very slowly; any rash means stop the drug and call, it may be Stevens-Johnson). Atypical antipsychotics (olanzapine, quetiapine, risperidone, aripiprazole) work fastest for acute agitation. ECT for refractory or pregnant patients.
4 · Who is involved?
  • Psychiatrist — stabilizer choice, level targets, decision about hospitalization or involuntary commitment when judgment is gone.
  • Nurse — the person who catches dehydration and exhaustion, sets limits, protects the other patients, and draws the trough level at the right hour.
  • Pharmacist — lithium interactions (NSAIDs, thiazides, ACE inhibitors), teratogenicity counseling, level interpretation.
  • Dietitian — portable calories, consistent sodium, weight tracking.
  • Therapist — CBT, interpersonal and social rhythm therapy (regularizing sleep and daily routine), adherence work.
  • Family — they see the prodrome first. Teach them the personal early-warning signs and give them a plan for who to call. Financial and legal protection during mania is part of family teaching.
5 · How can it get worse / be prevented?
  • 🚨 Lithium toxicity by level — memorize the ladder: Early (1.5–2.0): nausea, vomiting, diarrhea, coarse hand tremor, drowsiness, muscle weakness, slurred speech. Moderate (2.0–2.5): ataxia, blurred vision, tinnitus, giddiness, large output of dilute urine, worsening confusion. Severe (over 2.5): seizures, arrhythmias, hypotension, coma, death → hemodialysis. A fine tremor is an expected side effect; a coarse tremor is toxicity.
  • ⚠️ Long-term lithium: hypothyroidism (check TSH every 6 months), nephrogenic diabetes insipidus and reduced renal function (check creatinine), weight gain, acne, metallic taste.
  • 🚨 Antidepressant monotherapy can trigger mania or rapid cycling. Bipolar depression is treated with a stabilizer or quetiapine/lurasidone first. Never start an SSRI for a bipolar patient without a mood stabilizer on board.
  • 💀 Suicide risk is highest in the depressed and mixed states and during the crash right after mania. Reassess every shift; do not relax observation just because mania resolved.
  • ⚠️ Consequences of a single untreated episode: bankruptcy, DUI, job loss, divorce, unprotected sex and STIs, arrest. These are why early treatment matters, and they are also why patients grieve after an episode.
  • ✅ Teach: this is lifelong medication, feeling good is not a reason to stop; keep a mood and sleep chart; protect sleep as if it were a drug; no alcohol; carry a medical alert card for lithium; report tremor changes, vomiting, or diarrhea; and use effective contraception on valproate, carbamazepine, or lithium.
⭐ If you only remember one thing: In acute mania, the priority is the body — finger foods, fluids, sleep, low stimulation, because exhaustion kills before the mood does. For lithium: 0.6–1.2 therapeutic, over 1.5 is toxic, and anything that drops sodium or water (vomiting, diarrhea, sweating, NSAIDs, thiazides, low-salt diets) drives the level up.

🌧️ Major Depressive Disorder

One-line hook: pervasive, unrelenting low mood plus anhedonia for 2+ weeks — unlike grief, it does not come in waves, the self-esteem collapses, and nothing feels good in between. The dangerous moment is not the bottom; it is when the energy comes back.

1 · What is happening in the body?
  • Reduced serotonin, norepinephrine, and dopamine transmission — the monoamine theory. This explains why every first-line antidepressant raises one of the three.
  • HPA axis dysregulation with chronically elevated cortisol — this is why depression brings fatigue, poor concentration, appetite change, immune suppression, and real physical illness risk.
  • Loss of hippocampal volume and reduced neuroplasticity. Antidepressants raise neurotransmitters within hours but take 4–6 weeks to work because the actual repair is receptor and synapse remodeling, not the neurotransmitter bump. Teach this or she quits at week two.
  • Circadian disruption → early morning awakening, mood worst in the morning, and reversed sleep architecture.
  • Risk factors: family history, female sex, chronic medical illness, chronic pain, substance use, postpartum period, and loss.
  • Diagnosis: 5 or more SIG E CAPS symptoms for at least 2 weeks, and at least one must be depressed mood or anhedonia.
2 · How do you know?
  • SIG E CAPS: Sleep change · Interest lost (anhedonia) · Guilt/worthlessness · Energy gone · Concentration impaired · Appetite/weight change · Psychomotor agitation or retardation · Suicidal ideation.
  • 🧪 Tools: PHQ-9 (primary care standard — question 9 is the suicide item, act on it), Beck Depression Inventory, Hamilton Rating Scale, and the Geriatric Depression Scale for older adults.
  • Presentation traps: older adults present with memory complaints and somatic symptoms — pseudodementia; children and teens present as irritable and angry, not sad; men often present as anger, recklessness, or drinking.
  • Rule out the mimics: hypothyroidism, anemia, B12 deficiency, hypercalcemia, medication effects (beta blockers, steroids, interferon, isotretinoin), substance use, and — critically — a past manic episode.
  • 📈 Deterioration or emergency: not eating or drinking, catatonia, psychotic features (delusions of guilt, rot, or poverty), and any suicidal statement, giving away possessions, sudden calm, or an unexplained lift in mood.
  • Ask every depressed patient about suicide directly, at every contact — "Are you thinking about killing yourself?" Asking does not put the idea in their head; not asking leaves you blind.
3 · How do you fix it?
  • Safety is the first nursing priority, every shift. Then physical needs: fluids, food, sleep, hygiene, elimination. A severely depressed patient may not have the energy to drink water.
  • Approach: spend short, frequent, unhurried periods with them and do not demand cheerfulness. Sit in silence if that is what they can tolerate. Give one simple direction at a time, offer limited choices ("blue shirt or grey shirt"), and start with a task they can finish. Do not do everything for them; do not push beyond what they can do.
  • 💊 SSRIs are first line — sertraline, escitalopram, fluoxetine, paroxetine, citalopram. Side effects: GI upset, headache, insomnia or sedation, sexual dysfunction (the top reason patients quit), hyponatremia in older adults. Taper to stop — abrupt discontinuation causes flu-like discontinuation syndrome. Citalopram: QT prolongation, dose-capped.
  • 💊 SNRIs — venlafaxine (monitor blood pressure, it rises), duloxetine (also treats neuropathic pain). 💊 Bupropion — no sexual side effects and helps smoking cessation, but lowers the seizure threshold — contraindicated in seizure disorders and in eating disorders. 💊 Mirtazapine — sedating and increases appetite, so it is the pick for an older adult who is not sleeping or eating. 💊 TCAs (amitriptyline, nortriptyline) — effective but lethal in overdose from cardiac arrhythmia; dispense limited quantities to anyone at risk; heavy anticholinergic burden.
  • 💊 MAOIs — tyramine and the hypertensive crisis. Phenelzine, tranylcypromine, isocarboxazid, selegiline. Avoid all aged, fermented, cured, smoked, pickled, or spoiled foods: aged cheeses, salami/pepperoni/cured meats, smoked or pickled fish, liver, fermented soy — soy sauce, miso, tempeh, sauerkraut and kimchi, tap/draft beer and red wine, yeast extracts (Marmite/Vegemite), fava beans, overripe avocado or banana peel. Also avoid pseudoephedrine and other decongestants, dextromethorphan, meperidine, St. John's wort, and all other serotonergic drugs — 2-week washout between an MAOI and an SSRI, 5 weeks after fluoxetine. Crisis signs: sudden severe occipital (back-of-head) headache, spiking blood pressure, stiff neck, palpitations, nausea, sweating. Never combine an MAOI with an SSRI, SNRI, TCA, triptan, linezolid, or meperidine — that is serotonin syndrome, and never let a patient go home on an MAOI without a written food list.
  • ⚡ ECT — for treatment-resistant depression, psychotic depression, catatonia, pregnancy, and acute high suicide risk when you cannot wait 6 weeks. Consent required; NPO after midnight; remove dentures, glasses, hairpins, and jewelry; void first; give atropine (secretions), methohexital (anesthesia), succinylcholine (prevents injury from the convulsion). Afterward: side-lying position, monitor airway, reorient repeatedly — short-term memory loss and confusion are expected and usually resolve. Also: TMS, and ketamine/esketamine (works in hours; REMS program, monitor for 2 hours for sedation and dissociation).
4 · Who is involved?
  • Psychiatrist / primary care provider — diagnosis, medication trials, ECT referral, and ruling out thyroid and anemia first.
  • Nurse — suicide risk reassessment, med adherence and the 4–6 week expectation talk, ADL support, and the therapeutic presence that is itself an intervention.
  • Therapist — CBT and interpersonal therapy match medication for mild-to-moderate depression; combination beats either alone.
  • Pharmacist — MAOI diet counseling, serotonergic interaction screening, washout intervals, limited dispensing for TCAs.
  • Social worker — financial stress, housing, and the practical losses that keep the depression fed.
  • Family and peer support — teaching them to notice a sudden lift in mood, giving away belongings, or "getting affairs in order."
5 · How can it get worse / be prevented?
  • 🚨 The energy window. Suicide risk goes UP in the first 1–2 weeks of antidepressant treatment — psychomotor energy returns before mood and hopelessness lift, so now they have the drive to act on the plan they already had. Increase, do not decrease, observation as they start to look better.
  • 🚨 Black box warning: increased suicidal ideation in patients under 25. Weekly follow-up early in treatment.
  • 🚨 Serotonin syndrome — from combining serotonergic drugs. Fast onset (hours), hyperreflexia and clonus, agitation, diaphoresis, tremor, diarrhea, hyperthermia. Stop everything serotonergic, cool, benzodiazepines, cyproheptadine. Contrast with NMS: slow onset over days, lead-pipe rigidity, no clonus, no diarrhea, treated with dantrolene.
  • ⚠️ Other complications: hypertensive crisis on an MAOI, hyponatremia/SIADH on SSRIs in older adults, serotonin-related bleeding risk with NSAIDs or anticoagulants, weight gain, and untreated depression worsening cardiac and diabetic outcomes.
  • ⚠️ Relapse. Continue the antidepressant 6–12 months after remission for a first episode, and longer or indefinitely after recurrent episodes. Never let a patient stop an antidepressant abruptly or as soon as they feel better.
  • ✅ Teach: it takes 4–6 weeks — sleep and appetite improve first, mood last; take it daily, not PRN; no alcohol; report any thoughts of self-harm immediately; keep therapy appointments; exercise, light exposure, and sleep regularity have real antidepressant effect; and give family the crisis number (988 in the US).
⭐ If you only remember one thing: Ask about suicide directly, and watch hardest when the patient starts looking better — returning energy in weeks 1–2 of treatment is the peak-risk window. Antidepressants take 4–6 weeks; MAOIs mean no aged, fermented, or cured foods or you get a hypertensive crisis.

🌀 Generalized Anxiety Disorder

One-line hook: worry about everything, most days, for 6+ months — not the sudden 10-minute terror of a panic attack and not tied to one specific trigger like a phobia. The worry is constant, low-grade, and exhausting.

1 · What is happening in the body?
  • The amygdala (threat detector) is overactive and the prefrontal cortex cannot turn it off — the alarm keeps ringing with no fire.
  • Underactive GABA (the brain's brake) and dysregulated serotonin and norepinephrine. This is exactly why benzodiazepines — GABA enhancers — work within minutes, and why SSRIs take weeks.
  • Chronic sympathetic activation produces the physical symptoms directly: muscle tension, headaches, GI upset, fatigue, insomnia, and elevated heart rate. The body has been in low-grade fight-or-flight for months.
  • Sustained cortisol elevation → poor concentration, poor sleep, and real physical illness risk.
  • Peplau's four levels of anxiety describe what the brain can still do: mild (perception sharpened, learning is best here) → moderate (focus narrows, can be redirected) → severe (details only, cannot problem-solve) → panic (perception distorted, no rational thought, possible danger to self or others).
  • Highly comorbid with depression, other anxiety disorders, and substance use — alcohol is the most common form of self-medication.
2 · How do you know?
  • Excessive worry on more days than not for at least 6 months, about multiple areas (health, money, work, family), that the patient cannot control.
  • Plus 3 or more of 6: restlessness/on edge · easily fatigued · difficulty concentrating or mind going blank · irritability · muscle tension · sleep disturbance.
  • 🧪 Tools: GAD-7 (5 mild, 10 moderate, 15 severe), Hamilton Anxiety Rating Scale.
  • Physical presentation: they often come in for headaches, neck and shoulder tension, IBS symptoms, chest tightness, or insomnia, not for "anxiety."
  • Rule out: hyperthyroidism, hypoglycemia, pheochromocytoma, cardiac arrhythmia, caffeine, stimulants, and substance withdrawal — always check a TSH.
  • 📈 Assess which level of anxiety the patient is in right now, because the level dictates your intervention. You cannot teach relaxation techniques to a patient in severe or panic-level anxiety — they cannot process it; get them to moderate first with calm presence and simple direction.
3 · How do you fix it?
  • Match the intervention to the level: Panic/severe → stay with them, remain calm, low voice, short simple sentences, decrease stimuli, quiet area, do not leave them alone. Moderate → help them name what they feel and connect it to the trigger, then do a breathing exercise. Mild → now teach, problem-solve, and plan.
  • 💊 SSRIs and SNRIs are first line for long-term control — escitalopram, sertraline, paroxetine, venlafaxine, duloxetine. 4–6 weeks to full effect; anxiety can transiently worsen in the first week, so start low.
  • 💊 Buspirone — the anti-anxiety drug they love to test. No dependence, no sedation, no abuse potential, and no withdrawal — but it takes 2–4 weeks and must be taken daily. Never give buspirone PRN for an acute anxiety attack — it does nothing for hours or days, and never combine it with an MAOI.
  • 💊 Benzodiazepines (lorazepam, alprazolam, diazepam, clonazepam) — fast but short-term only (2–4 weeks) because of tolerance, dependence, and rebound anxiety. Fall risk and confusion in older adults; never with alcohol or opioids — additive respiratory depression. Taper, never stop abruptly — withdrawal can cause seizures. Reversal agent is flumazenil.
  • 💊 Adjuncts: hydroxyzine (non-addictive PRN option), propranolol for performance anxiety and physical symptoms. Antihistamines and beta blockers do not treat the disorder, only the symptoms.
  • 🧘 Non-drug, and just as important: CBT is at least as effective as medication; diaphragmatic breathing, progressive muscle relaxation, mindfulness, regular aerobic exercise, sleep hygiene, and cutting caffeine, nicotine, and energy drinks. Journaling to identify triggers.
4 · Who is involved?
  • Primary care provider — most GAD is diagnosed and treated here; rules out thyroid and cardiac causes.
  • Psychiatrist — refractory cases, comorbid depression, tapering a patient off long-term benzodiazepines.
  • Therapist — CBT, exposure to feared outcomes, worry-postponement techniques.
  • Nurse — assess the anxiety level, provide calm presence, teach breathing and relaxation at the right moment, and reinforce that buspirone and SSRIs are not rescue drugs.
  • Pharmacist — benzodiazepine risk counseling, taper schedules, interaction checks.
  • Family — teach them that reassurance-seeking is a symptom; endlessly reassuring feeds the loop.
5 · How can it get worse / be prevented?
  • 🚨 Benzodiazepine withdrawal is dangerous — abrupt discontinuation causes rebound anxiety, insomnia, tremor, and seizures. Always taper. The same physiology as alcohol withdrawal, because both act on GABA.
  • ⚠️ Substance use disorder — self-medication with alcohol, cannabis, or diverted benzodiazepines is common. Screen every anxious patient.
  • ⚠️ Untreated GAD leads to major depression, chronic insomnia, IBS, tension headaches, hypertension, and functional decline — job loss and social withdrawal.
  • ⚠️ Avoidance makes anxiety worse. Every time the patient escapes the feared situation, the relief reinforces the fear. This is why exposure, not avoidance, is the treatment.
  • ✅ Teach: take the SSRI or buspirone daily, not PRN; expect 2–6 weeks; do not stop abruptly; limit caffeine and alcohol; keep a regular sleep schedule; use the breathing technique before anxiety peaks, not after; and exercise most days.
  • ✅ Teach family: help the patient name the feeling instead of fixing the problem, do not take over their tasks, and expect progress to be gradual.
⭐ If you only remember one thing: Assess the anxiety level first, because it decides your intervention — teaching and problem-solving only work at mild-to-moderate; at severe or panic you stay, stay calm, use short sentences, and reduce stimuli. Buspirone is daily and takes weeks; it is never a rescue drug.

💥 Panic Disorder

One-line hook: a discrete attack that slams to peak within 10 minutes and burns out in under 30, feels like dying, and comes out of nowhere — that abrupt on/off is what separates it from GAD's constant hum. Rule out the heart before you call it panic.

1 · What is happening in the body?
  • A massive, sudden sympathetic (catecholamine) surge with no external threat — a full fight-or-flight response fired by mistake.
  • That surge explains every symptom mechanically: tachycardia and palpitations, chest tightness, hyperventilation, sweating, tremor, dilated pupils, GI shutdown, and cold extremities.
  • Hyperventilation blows off CO₂ → respiratory alkalosis → tingling in the fingers and around the mouth, lightheadedness, and carpal spasm. This is why slow breathing, not oxygen, is the fix.
  • Overactive amygdala plus a hypersensitive brainstem suffocation alarm; low GABA and dysregulated serotonin and norepinephrine.
  • The fear-of-fear cycle: a benign body sensation is catastrophically misread ("my heart is racing, I'm having a heart attack"), the alarm fires, symptoms intensify, and the interpretation is confirmed.
  • Avoidance of places where an attack happened → agoraphobia, which is what actually shrinks the patient's life.
2 · How do you know?
  • Recurrent unexpected panic attacks plus at least 1 month of persistent worry about more attacks or a maladaptive change in behavior to avoid them.
  • Attack symptoms (4 or more): palpitations, sweating, trembling, shortness of breath or smothering, choking sensation, chest pain, nausea, dizziness, chills or hot flushes, paresthesias, derealization or depersonalization, fear of losing control or going crazy, fear of dying.
  • ⏱️ Peaks within 10 minutes, typically resolves in 20–30 minutes, and leaves the patient wrung out and exhausted.
  • 🚨 Panic attacks mimic MI, PE, arrhythmia, hypoglycemia, hyperthyroidism, asthma, and stimulant intoxication. Rule out the cardiac and respiratory causes before diagnosing panic — ECG, troponin, glucose, TSH, tox screen. Panic disorder is never the first-visit diagnosis in a new-onset chest pain patient.
  • During the attack the patient is at panic-level anxiety: cannot follow directions, cannot problem-solve, perception is distorted. Assess by what they can do, not what they say.
  • 📈 Deterioration: increasing avoidance, refusing to leave home, missing work, escalating alcohol or benzodiazepine use, and emerging depression or suicidal ideation.
3 · How do you fix it?
  • During an attack — the tested answer is: stay with the patient. Never leave a patient alone during a panic attack. Your calm presence is the intervention.
  • Use a calm, low, firm voice and very short simple sentences. "You are safe. I am staying here. Breathe with me." Repeat as needed. Do not ask open-ended or complex questions, do not try to explore the cause, and do not teach anything — they cannot process it right now.
  • Move them to a smaller, quieter, less stimulating area and stay with them. Ask before touching — touch can feel threatening at panic level.
  • Slow their breathing by modeling it — have them breathe with you, in through the nose and out slowly. Slow breathing corrects the respiratory alkalosis that is producing the tingling and dizziness. Grounding helps: name 5 things you can see.
  • 💊 Acute: a short-acting benzodiazepine (lorazepam, alprazolam) breaks the attack. Maintenance: SSRIs are first line (sertraline, paroxetine, escitalopram) — start at a very low dose because they can transiently worsen panic, then titrate up. Venlafaxine is an alternative. Goal is to get the patient off benzodiazepines.
  • 🧠 CBT with interoceptive exposure is the definitive treatment — the patient deliberately reproduces the sensations (spinning, breathing through a straw, running in place) until the body sensation stops meaning danger. Combined with graded exposure for agoraphobia.
4 · Who is involved?
  • Emergency department — frequently the first contact; must exclude MI, PE, and arrhythmia before anyone says "it's just anxiety."
  • Primary care provider — the workup, the TSH and glucose, and starting the SSRI.
  • Psychiatrist — refractory panic, benzodiazepine tapering, comorbid depression.
  • Therapist — CBT, interoceptive and in vivo exposure, cognitive restructuring of the catastrophic interpretation.
  • Nurse — the person present during the attack; also the one who teaches the breathing plan afterward, when the patient can actually learn.
  • Family — teach them what to do during an attack (stay, stay calm, do not add stimulation, do not drive them to the ER every time) and what not to do (take over their avoidance for them).
5 · How can it get worse / be prevented?
  • 🚨 Agoraphobia — the biggest functional complication. Avoidance spreads from one place to many until the patient is housebound. Every accommodation the family makes reinforces it.
  • 🚨 Substance use and benzodiazepine dependence — panic patients are at high risk of self-medicating with alcohol and of escalating PRN benzodiazepine use. Tolerance develops and withdrawal can cause seizures.
  • ⚠️ Depression and suicide risk rise with untreated panic disorder — ask directly.
  • ⚠️ Repeated ER visits, unnecessary cardiac workups, job loss, and financial strain. Some patients also start to genuinely believe they have an undiagnosed heart condition.
  • ✅ Teach the patient: a panic attack cannot kill you and it will end on its own; the symptoms are adrenaline, not a heart attack; practice the breathing daily when calm so it is automatic when it is not; do not avoid the places where attacks happened; cut caffeine, nicotine, and stimulants; keep regular sleep; and take the SSRI daily even on good days.
  • ✅ Teach: report any new or different chest pain rather than assuming it is panic — panic patients get cardiac disease too.
⭐ If you only remember one thing: Stay with the patient, stay calm, short simple sentences, quiet space, breathe with them — and save all teaching for after the attack. Peaks in 10 minutes; rule out cardiac causes first.

🌩️ PTSD

One-line hook: the trauma is over but the brain keeps replaying it as if it is happening now — and it must last more than 1 month. Under 1 month with the same picture is acute stress disorder.

1 · What is happening in the body?
  • The amygdala is stuck on, the prefrontal cortex cannot override it, and the hippocampus (which timestamps memories) is reduced in volume. That last piece is why the memory has no "past" tag — a flashback feels like present tense, not recall.
  • Dysregulated cortisol and a hair-trigger norepinephrine system → the startle response, the scanning, the insomnia, and the nightmares.
  • Conditioned associations form to sights, sounds, and smells present at the trauma. A slammed door or a specific cologne can fire the whole alarm without any conscious thought.
  • Requires exposure to actual or threatened death, serious injury, or sexual violence — directly experienced, witnessed, learned of in a close other, or repeated exposure to details (first responders, ICU nurses).
  • Risk is higher with interpersonal and repeated trauma (assault, combat, childhood abuse) than with a single natural disaster, and higher with poor social support afterward.
  • Timeline matters: under 3 days = acute stress reaction · 3 days to 1 month = acute stress disorder · over 1 month = PTSD · onset more than 6 months later = delayed expression.
2 · How do you know?
  • Four symptom clusters, all four required:
    • Intrusion — flashbacks, nightmares, intrusive memories, intense distress at reminders.
    • Avoidance — of people, places, conversations, thoughts, and feelings connected to the trauma.
    • Negative alterations in cognition and mood — amnesia for part of the event, persistent shame or guilt, "the world is dangerous," detachment, anhedonia, survivor guilt.
    • Arousal and reactivity — hypervigilance, exaggerated startle, irritability or anger outbursts, reckless behavior, poor concentration, sleep disturbance.
  • 🧪 Tools: PCL-5, PC-PTSD-5 screen, CAPS-5 (clinician-administered gold standard).
  • A flashback is a dissociative re-experiencing — the patient is not oriented to the room, they are back in the event. Do not mistake it for psychosis; do not mistake it for noncompliance.
  • Look for the comorbidities, because they are the rule: depression, substance use disorder, other anxiety disorders, chronic pain, and traumatic brain injury.
  • 📈 Deterioration: escalating alcohol or opioid use, self-harm, rage episodes, increasing isolation, and suicidal ideation — PTSD carries a substantially elevated suicide risk.
  • ⚠️ Screen every patient for current safety if the trauma is ongoing (intimate partner violence, human trafficking) — you cannot treat trauma the patient is still living in. Interview alone, without the partner present.
3 · How do you fix it?
  • During a flashback — ground them in the present. Stay calm, say your name and role, tell them where they are and that they are safe now, and state the year. Use 5-4-3-2-1 grounding (5 things you see, 4 you hear, 3 you touch...) or have them feel their feet on the floor and describe the room. Never touch a patient in a flashback without asking first, and never approach from behind or corner them — you can be incorporated into the trauma.
  • Trauma-informed care is the framework: explain everything before you do it, ask permission, offer choices and control wherever possible, minimize surprises, keep the door accessible, and let the patient pick where they sit. Control is what was taken from them; giving it back is the intervention.
  • Let the patient set the pace of disclosure. Do not press for details, do not ask them to "tell me exactly what happened" to satisfy your own curiosity, and do not say "I understand" or "at least you survived." Reflect and validate: "That sounds terrifying. You're safe here."
  • 🧠 Trauma-focused psychotherapy is first-line, ahead of medication: prolonged exposure, cognitive processing therapy (CPT), trauma-focused CBT, and EMDR. These work; general supportive counseling alone does not.
  • 💊 SSRIs — sertraline and paroxetine are FDA approved for PTSD; venlafaxine is also effective. Expect 4–6 weeks (often 8–12 for PTSD). 💊 Prazosin — an alpha-1 blocker given at bedtime specifically for trauma nightmares and sleep disturbance; monitor for orthostatic hypotension and first-dose syncope, teach them to rise slowly.
  • 💊 Avoid benzodiazepines in PTSD — they do not treat it, they interfere with the extinction learning that exposure therapy depends on, and this population has high substance-use risk. Also avoid pushing debriefing sessions immediately after a trauma; single-session critical incident debriefing can worsen outcomes.
4 · Who is involved?
  • Trauma-trained therapist — CPT, prolonged exposure, or EMDR. This is the treatment, not an add-on.
  • Psychiatrist / prescriber — SSRI, prazosin for nightmares, and managing the comorbid depression and substance use.
  • Nurse — grounding during flashbacks, trauma-informed procedure practice, sleep and safety assessment, and screening for ongoing abuse.
  • Substance use counselor — PTSD and substance use disorder must be treated together; treating only one causes relapse in both.
  • Social worker / victim advocate — safety planning, shelter, legal advocacy, protective orders, disability and VA benefits.
  • Peer support — veteran groups, survivor groups. Being believed by someone with the same history does something clinical care cannot.
5 · How can it get worse / be prevented?
  • 🚨 Suicide — the most serious complication, driven by hopelessness, guilt, insomnia, and substance use. Ask directly and repeatedly.
  • 🚨 Substance use disorder — alcohol, cannabis, and opioids used to blunt hyperarousal and stop the nightmares. This is the most common self-treatment and the most common way PTSD gets worse.
  • ⚠️ Avoidance is the engine of chronicity. Every avoided reminder prevents the extinction learning that would let the fear fade. Untreated PTSD can persist for decades.
  • ⚠️ Relationship breakdown, job loss, legal problems from anger outbursts, chronic insomnia, hypertension and cardiovascular disease, and re-traumatization by health care itself (restraints, pelvic exams, intubation, being held down).
  • ✅ Prevention and teaching: early social support and early trauma-focused therapy reduce chronicity; keep a regular sleep schedule; no alcohol as a sleep aid — it fragments sleep and worsens nightmares; exercise; practice grounding daily so it is available in a crisis; identify triggers and plan for predictable ones (fireworks, anniversaries).
  • ✅ Teach family: do not startle them awake or approach from behind, do not push them to "get over it," expect anniversary reactions, and learn the grounding script so they can use it too.
⭐ If you only remember one thing: Flashback = ground them in the here and now (your name, this place, this year, feet on the floor) and do not touch without asking. Trauma-focused therapy first, SSRIs second, prazosin for nightmares, and benzodiazepines are the wrong answer.

🔁 OCD

One-line hook: the obsession creates the anxiety and the compulsion is the only thing that turns it off — that is why taking the ritual away without treating the anxiety causes panic. The patient knows it makes no sense; that is the difference from a delusion.

1 · What is happening in the body?
  • A hyperactive cortico-striatal-thalamo-cortical loop — the brain circuit that says "something is wrong, act on it" fires and will not shut off. The signal keeps looping instead of being marked "done."
  • Serotonin dysregulation — which is why serotonergic drugs work, but at higher doses and over a longer time than in depression.
  • The negative reinforcement trap: the obsession raises anxiety → the compulsion drops it briefly → the brain learns "the ritual is what keeps me safe" → the urge returns stronger. Every completed ritual makes the next obsession louder.
  • The patient generally has insight — they know the fear is irrational and are ashamed of it, which is why OCD is often hidden for years.
  • PANDAS — abrupt-onset OCD and tics in a child after a group A streptococcal infection, from an autoimmune reaction.
  • Related disorders in the same family: body dysmorphic disorder, hoarding disorder, trichotillomania (hair pulling), and excoriation (skin picking).
2 · How do you know?
  • Obsessions = recurrent, intrusive, unwanted thoughts, images, or urges that cause marked anxiety — contamination, doubt ("did I lock it?"), symmetry, forbidden aggressive or sexual thoughts, fear of harming someone. The patient does not want these thoughts; they are ego-dystonic.
  • Compulsions = repetitive behaviors or mental acts done to neutralize the obsession — washing, checking, counting, ordering, repeating, praying, seeking reassurance.
  • Diagnostic threshold: more than 1 hour per day, or clinically significant distress and functional impairment.
  • 🧪 Tool: Y-BOCS (Yale-Brown Obsessive Compulsive Scale) — measures time spent, distress, interference, resistance, and control, and is used to track treatment response.
  • Physical evidence to assess: raw, cracked, bleeding hands from washing, skin breakdown, bald patches, dental damage, and severe sleep loss from rituals running into the night.
  • 📈 Deterioration: rituals expanding in time, family members being recruited into the rituals, inability to leave the house or get to work, weight loss, and comorbid depression and suicidal ideation — which are common and often the reason they finally present.
3 · How do you fix it?
  • At first, allow the ritual and build in time for it. Never abruptly stop or interrupt a compulsion — the anxiety it was containing floods back and the patient panics. Wake the patient earlier so the morning ritual does not make them late; that is a legitimate nursing intervention.
  • Then set limits gradually and collaboratively, with the patient's agreement — reduce the ritual by a set amount, structure the day with scheduled activities that compete with ritual time, and reinforce every non-ritual behavior.
  • Do not shame, argue, or call the ritual silly, and do not participate in it or provide the reassurance they are seeking — reassurance is itself a compulsion and giving it feeds the loop. Acknowledge the distress instead: "I know the thought is frightening. I'll sit with you while it passes."
  • 🧠 ERP — Exposure and Response Prevention — is the gold-standard treatment. The patient is exposed to the trigger (touch the doorknob) and then prevented from performing the ritual, and stays there until anxiety comes down on its own. That is the learning: anxiety falls without the compulsion. Delivered by a trained therapist, in a graded hierarchy.
  • 💊 SSRIs — first line, but note the two differences from depression: higher doses and 10–12 weeks to full effect. Fluoxetine, fluvoxamine, sertraline, paroxetine. Do not call it a failure at 4 weeks.
  • 💊 Clomipramine (a TCA, strongly serotonergic) is highly effective and often used when SSRIs fail — but carries anticholinergic effects, orthostatic hypotension, seizure risk, and lethality in overdose. Antipsychotic augmentation for refractory cases; deep brain stimulation in extreme, treatment-resistant OCD.
  • 🩹 Do not forget the body: treat the skin — mild soap, moisturizer, wound care for washing injuries — and monitor nutrition and sleep.
4 · Who is involved?
  • Therapist trained in ERP — this is the essential team member; generic talk therapy does not treat OCD.
  • Psychiatrist — high-dose SSRI trials, clomipramine, augmentation strategies.
  • Nurse — schedule structuring, ritual time allowance, skin assessment and care, anxiety support during response prevention, and monitoring for depression and suicide risk.
  • Pharmacist — the long timeline and higher-than-usual dosing, drug interactions (fluvoxamine is a potent inhibitor of many drugs), TCA overdose risk.
  • Family — teach them to stop accommodating: no more buying extra soap, no more answering the same reassurance question, no more performing checks for the patient. Family accommodation is one of the strongest predictors of poor outcome.
  • School / employer — accommodations for time-consuming symptoms during treatment.
5 · How can it get worse / be prevented?
  • 🚨 Severe skin breakdown and infection from compulsive washing, and dehydration or malnutrition when rituals crowd out eating.
  • 🚨 Depression and suicide — roughly two-thirds of OCD patients develop major depression; assess suicide risk directly, especially in severe or treatment-resistant cases.
  • ⚠️ Complete functional collapse — homebound, unemployed, estranged; the whole household reorganized around the rituals.
  • ⚠️ Relapse after stopping medication is high — maintain the SSRI for at least 1–2 years after remission, and taper slowly. Symptoms also flare under stress, sleep deprivation, and illness.
  • ✅ Teach the patient: having the thought does not mean you want it or will act on it — this is the single most relieving thing you can say to someone with aggressive or taboo obsessions; the medication takes 10–12 weeks and needs a higher dose; ERP feels worse before it feels better and that is the mechanism working; do not use alcohol to blunt the anxiety.
  • ✅ Teach: relapse signs are rituals creeping back and reassurance-seeking restarting — go back to the ERP tools early rather than waiting for full relapse.
⭐ If you only remember one thing: Do not take the ritual away abruptly — allow it and schedule around it at first, then reduce it gradually. ERP is the gold standard, and OCD needs higher SSRI doses for 10–12 weeks. Do not give the reassurance they ask for; it is part of the compulsion.

⚡ Borderline Personality Disorder

One-line hook: instability is the diagnosis — relationships, identity, mood, and impulse control all swing, driven by a terror of abandonment. Unlike bipolar, the mood shifts happen within hours and are triggered by relationships, not by a weeks-long episode.

1 · What is happening in the body?
  • A hyperreactive amygdala plus an underactive prefrontal cortex — emotions spike faster, higher, and take much longer to come back down than in other people. This is a genuine emotion-regulation deficit, not manipulation for its own sake.
  • Strong association with childhood trauma, abuse, neglect, and invalidating environments — a child whose feelings were repeatedly dismissed never learns to name or soothe them.
  • Splitting is the core defense: people and situations are all good or all bad, with no middle. The same nurse is the only one who understands on Monday and the cruelest person on the unit on Tuesday. It is a protection against the terrifying idea that someone you need can also disappoint you.
  • Other defenses: projection, projective identification, idealization/devaluation, and acting out.
  • Self-harm usually serves a function — to end emotional numbness, to convert unbearable emotional pain into physical pain, or to regain a sense of control. It is often not an attempt to die, but it is still a real risk and must be assessed every time.
  • Onset is by adolescence or early adulthood and is pervasive across situations — that is what makes it a personality disorder rather than a mood episode.
2 · How do you know?
  • Frantic efforts to avoid real or imagined abandonment — the organizing fear. A cancelled appointment can trigger a crisis.
  • Unstable, intense relationships that swing between idealization and devaluation; unstable self-image and chronic feelings of emptiness.
  • Impulsivity in at least two self-damaging areas — spending, sex, substance use, reckless driving, binge eating.
  • Recurrent self-mutilation, suicidal gestures, or threats; affective instability lasting hours (not weeks); inappropriate intense anger; and transient stress-related paranoia or dissociation.
  • On the unit: staff splitting is visible in the chart and in report — some staff insist the patient is doing great, others find them impossible. When staff members strongly disagree about a patient, suspect splitting and take it to the team, not to the patient.
  • 📈 Deterioration: escalating self-harm, threats tied to a specific person leaving, increasing dissociation, substance use, and true suicide attempts — about 8–10% die by suicide, so never dismiss a gesture as attention-seeking.
3 · How do you fix it?
  • Consistency is the treatment. The whole team uses the same clear, written, realistic limits, communicated to every shift and to the patient. Inconsistency between staff is what splitting feeds on. Hold a team meeting; document the plan; do not negotiate individually.
  • Set limits matter-of-factly, without anger or moralizing. State the behavior, the limit, and the consequence once. Do not argue, do not defend yourself, do not get pulled into a debate about fairness.
  • Maintain clear professional boundaries. Never accept gifts, share personal information, give out your phone number, agree to be "the only one who understands," or make exceptions to unit rules for this patient — every special exception confirms the split and sets up the crash.
  • Respond to self-harm calmly and clinically: assess and treat the injury, assess suicidal intent every time, then give the attention to the feelings and coping, not to the wound. Do not lecture, do not act horrified, and do not give extra nursing time as a reward for the injury. Encourage them to come to staff before harming.
  • 🧠 DBT (Dialectical Behavior Therapy) is the evidence-based treatment — Marsha Linehan's four skill modules: mindfulness · distress tolerance · emotion regulation · interpersonal effectiveness. It reduces self-harm and hospitalization. Also effective: mentalization-based therapy, schema therapy.
  • 💊 No medication treats BPD itself. Medications target specific symptoms only — SSRIs for mood and impulsivity, mood stabilizers for anger and lability, low-dose antipsychotics for transient paranoia or dissociation. Prescribe cautiously and in limited quantities because of overdose risk.
4 · Who is involved?
  • The whole nursing team acting as one — regular team meetings to compare notes are the anti-splitting intervention. This is arguably the most important item on the list.
  • DBT-trained therapist — individual therapy plus skills group; the group is where the skills are actually learned.
  • Psychiatrist — targeted symptom medication, limited dispensing, and deciding when hospitalization helps versus when it reinforces the crisis pattern.
  • Primary/consistent case manager — one point of contact reduces the number of relationships that can be split.
  • Family — psychoeducation and family DBT skills; teach validation without capitulation, and how to respond to threats safely.
  • Emergency and crisis services — a written crisis plan with named steps and phone numbers, agreed on when the patient is calm.
5 · How can it get worse / be prevented?
  • 🚨 Completed suicide in roughly 8–10% — the highest of any personality disorder. Assess intent, plan, and means at every episode of self-harm. Never label a self-harm episode as "just attention-seeking" and skip the risk assessment.
  • 🚨 Escalating self-injury and dissociation, unintentionally lethal injury, and infection or scarring from repeated cutting or burning.
  • ⚠️ Substance use disorder and eating disorders are highly comorbid and multiply the risk of both self-harm and accidental death.
  • ⚠️ Iatrogenic worsening — repeated hospitalizations, staff burnout and rejection, and inconsistent limits all reinforce the illness. Being disliked by staff is a clinical event with clinical consequences here.
  • ✅ Realistic prognosis to teach: BPD improves substantially with treatment and with age — many patients no longer meet criteria after several years of DBT. That is a hopeful and true message.
  • ✅ Teach the patient: use the distress-tolerance skill before the crisis peaks (ice, paced breathing, intense exercise); call the crisis line or come to staff before self-harming; keep the same therapist; expect setbacks. Teach family: validate the feeling ("that would hurt"), hold the limit anyway, do not threaten to leave in an argument, and remove firearms and stockpiled medications from the home.
⭐ If you only remember one thing: Consistent limits from a united team is the intervention — splitting only works when staff disagree. DBT is the evidence-based therapy, no drug treats the disorder itself, and every self-harm episode gets a real suicide risk assessment.

🍽️ Anorexia Nervosa

One-line hook: restriction to a significantly low body weight, with terror of gaining and a distorted body image — and it has the highest mortality of any psychiatric illness, from cardiac arrest and suicide. The nursing priority is never the eating; it is the heart.

1 · What is happening in the body?
  • Starvation physiology. The body burns glycogen, then fat, then muscle — including cardiac muscle. The heart shrinks and the conduction system becomes unstable.
  • Compensatory hypometabolism: bradycardia, hypotension, hypothermia, and lanugo (fine downy hair to conserve heat) are the body trying to spend less energy. Bradycardia here is a danger sign, not fitness.
  • Hypothalamic-pituitary shutdown → low estrogen, amenorrhea, low T3, and osteoporosis that may not fully reverse.
  • Psychologically: control. When everything else feels unmanageable, intake is the one thing that can be controlled absolutely — which is why food battles fail and control-restoring interventions work.
  • Two subtypes: restricting type and binge-eating/purging type. Anorexia patients can purge too — the difference from bulimia is the low body weight.
  • Frequently comorbid with OCD, perfectionism, anxiety, and depression; onset typically in adolescence.
2 · How do you know?
  • Three criteria: restriction leading to significantly low weight for age/sex/development · intense fear of gaining weight or persistent behavior that prevents gain · disturbance in how body weight is experienced, or denial of the seriousness of the low weight.
  • 🫀 Cardiac findings are the ones that kill: bradycardia (often under 50), hypotension, orthostatic changes, arrhythmias, prolonged QT, and peripheral edema. Get an ECG.
  • 🧪 Labs: hypokalemia, hypomagnesemia, hypophosphatemia, hyponatremia, elevated BUN and creatinine (dehydration), low albumin, anemia and leukopenia, elevated liver enzymes, low T3, elevated cortisol, and bone density loss on DEXA.
  • Physical: lanugo, dry cracked skin, brittle hair and hair loss, cold mottled extremities, amenorrhea, delayed gastric emptying and constipation, muscle wasting.
  • Behavior to observe: cutting food into tiny pieces, moving it around the plate, hiding food in napkins or pockets, excessive exercise, wearing baggy layers, ritualized eating, obsessive calorie and weight tracking, and water loading before weigh-ins.
  • 📈 Admit / escalate for: heart rate under 40–50, systolic BP under 80–90, temperature under 96°F, potassium or phosphorus critically low, arrhythmia, syncope, weight below roughly 75% of expected, or acute suicide risk.
3 · How do you fix it?
  • Priority order: cardiac and fluid/electrolyte stabilization → nutritional restoration → then the psychological work. You cannot do therapy with a starved brain — cognition improves only after weight restores.
  • 🚨 Refeeding syndrome is the thing to fear when you start feeding them. Insulin surges as carbohydrates return and drives phosphate, potassium, and magnesium into cells. Hypophosphatemia is the hallmark of refeeding syndrome and it causes heart failure, arrhythmias, respiratory failure, rhabdomyolysis, seizures, and death. Prevent it: start low and advance slowly, give thiamine before/with feeding, and check phosphorus, potassium, and magnesium daily during early refeeding. Watch for edema and rising weight from fluid, not tissue.
  • Weighing protocol — they test this: same scale, same time each morning, after voiding, before eating, in a gown or the same clothing, back to the scale. Check pockets for hidden weights and assess for water loading. Weigh no more often than the plan specifies.
  • Mealtime nursing: supervise meals and remain with the patient for 1 hour afterward with the bathroom off limits, to prevent purging and food disposal. Set a time limit for the meal. Be matter-of-fact — do not argue, bargain, beg, or comment on the food or the body. If the patient will not eat, the agreed consequence (supplement, then enteral feeding) follows without debate.
  • Therapeutic approach: give control back where it is safe (choosing between two menus, choosing the order of activities), praise effort and non-food accomplishments, never appearance. Explore the feelings underneath — "what were you feeling before dinner?" Use a behavioral contract with clear privileges tied to weight and intake goals, agreed in advance.
  • 💊 No medication is approved to treat anorexia. Olanzapine is sometimes used for extreme rigidity and to support weight gain; SSRIs help the comorbid depression and OCD but only after weight is restored (they do not work in a starved brain). Family-Based Treatment (Maudsley) is first-line for adolescents; CBT-E for adults.
4 · Who is involved?
  • Medical provider — cardiac monitoring, electrolyte replacement, refeeding orders, bone density, and deciding the level of care.
  • Registered dietitian — the calorie prescription, the meal plan advancement, and being the one who owns the numbers so the nurse-patient relationship is not a food fight.
  • Nurse — vital signs and rhythm, daily weights done correctly, meal supervision and the post-meal hour, electrolyte trends, and the therapeutic relationship.
  • Therapist — CBT-E, family-based treatment, body image work, and treating the underlying anxiety and perfectionism.
  • Family — in adolescents the parents are given temporary control of refeeding (Maudsley); in all cases they need teaching not to comment on weight, appearance, or dieting.
  • Psychiatrist — comorbid depression, OCD, and suicide risk, which is substantial in this population.
5 · How can it get worse / be prevented?
  • 🚨 Cardiac arrest from arrhythmia — driven by hypokalemia, hypomagnesemia, and prolonged QT. This plus suicide is why anorexia has the highest mortality in psychiatry (roughly 5–10%).
  • 🚨 Refeeding syndrome — falling phosphorus, potassium, and magnesium in the first days of nutrition. Never advance calories rapidly in a severely malnourished patient, and never skip the daily phosphorus check during early refeeding.
  • ⚠️ Irreversible complications: osteoporosis and fractures, growth stunting, infertility, and structural brain changes. Early treatment is the only prevention.
  • ⚠️ Other: severe constipation and gastroparesis, esophageal tears if purging, dental erosion, anemia, immunosuppression, and suicide — the second leading cause of death here. Assess suicide risk directly.
  • ✅ Teach: weight restoration comes before the thinking changes, not after; the initial weight gain is partly fluid and it feels awful but it is expected; edema is temporary; recovery is not linear; relapse warning signs are re-counting calories, skipping meals, and returning exercise rituals.
  • ✅ Teach family: no comments about weight, food, dieting, or bodies — including their own; do not police, do not plead; eat together; and keep every follow-up appointment because relapse rates are high in the first year.
⭐ If you only remember one thing: The priority is cardiac — bradycardia, hypotension, hypokalemia, prolonged QT. When you start feeding, watch for refeeding syndrome, whose hallmark is a falling phosphorus. Weigh same time, same scale, after voiding, gown on, back to the scale, and stay with the patient for 1 hour after meals.

🦷 Bulimia Nervosa

One-line hook: binge then purge, at a normal or slightly above-normal weight — which is exactly why it gets missed for years. The tell is on the teeth, the knuckles, and the potassium.

1 · What is happening in the body?
  • The binge-purge cycle is self-reinforcing: restriction and hunger → loss of control binge → shame and panic about calories → purge → temporary relief → renewed restriction. Restriction is what sets up the next binge.
  • Vomiting loses hydrogen and chloride → hypokalemic, hypochloremic metabolic alkalosis and dehydration. Laxative abuse loses bicarbonate through the gut → metabolic acidosis instead. Same disorder, opposite acid-base picture depending on the route.
  • Potassium is the dangerous loss — from vomiting, from diuretic and laxative abuse, and from the aldosterone response to volume depletion. Hypokalemia causes the fatal arrhythmias.
  • Gastric acid on the teeth and esophagus explains the enamel erosion, dental caries, esophagitis, and Mallory-Weiss tears; repeated stimulation of the salivary glands explains the parotid swelling.
  • Serotonin dysregulation and high impulsivity — which is why bulimia runs with substance use, self-harm, and borderline traits far more than anorexia does.
  • These patients usually feel shame and want to stop, in contrast to anorexia where the behavior often feels like an achievement. That difference makes them more treatable.
2 · How do you know?
  • Criteria: recurrent binge eating (an objectively large amount in a discrete period, with a sense of loss of control) plus recurrent inappropriate compensatory behavior, both at least once a week for 3 months, with self-evaluation unduly influenced by shape and weight — and not occurring only during anorexia.
  • Compensation routes: self-induced vomiting, laxatives, diuretics, enemas, fasting, insulin omission in type 1 diabetes, and excessive exercise.
  • 🔎 The physical tells: Russell's sign (calluses or scars on the knuckles from inducing vomiting) · dental enamel erosion on the inner surfaces and rampant caries · bilateral parotid gland swelling giving a puffy jaw · sore throat, hoarseness, and conjunctival hemorrhages from retching.
  • 🧪 Labs: hypokalemia (the critical one), hypochloremia, metabolic alkalosis from vomiting or metabolic acidosis from laxatives, hypomagnesemia, dehydration, and elevated amylase.
  • Behavior: disappearing to the bathroom right after meals, running water or showers after eating, large amounts of food missing, laxative or diet-pill packaging, secretive eating, and intense shame when asked.
  • 📈 Deterioration: potassium falling, arrhythmias or palpitations, syncope, hematemesis (Mallory-Weiss tear), escalating laxative doses, and rising self-harm or suicidal ideation.
3 · How do you fix it?
  • Priority: correct the electrolytes. Hypokalemia is what stops the heart — replace potassium, put them on telemetry if severe, check magnesium too (you cannot correct potassium with a low magnesium), and get an ECG for QT.
  • Interrupt the cycle with structure: three planned meals plus snacks at regular times, no skipping and no dieting — regular eating is the single most effective behavioral change because it removes the hunger that drives the binge.
  • Observe during and for 1–2 hours after meals, with the bathroom unavailable or supervised, to interrupt purging. Do it as a stated part of the plan, not as a gotcha.
  • Approach: matter-of-fact and non-judgmental. These patients are already drowning in shame — do not express disgust, do not lecture, and do not make the binge the whole conversation. Explore the trigger and the feeling that preceded it, and help them find a substitute behavior for that moment. A food and feelings diary is the standard tool.
  • 💊 Fluoxetine is the only FDA-approved medication for bulimia, at 60 mg — a higher dose than for depression. It reduces binge and purge frequency. Never give bupropion to a patient with bulimia or anorexia — it markedly lowers the seizure threshold in purging patients and is contraindicated.
  • 🧠 CBT is the gold-standard psychotherapy (CBT-E), with interpersonal therapy as an alternative. Add dental referral early, because the enamel damage is permanent and progressive.
4 · Who is involved?
  • Medical provider — electrolytes, ECG and QT, telemetry decisions, esophageal evaluation for bleeding.
  • Nurse — potassium and rhythm monitoring, meal and post-meal observation, oral assessment, non-judgmental therapeutic presence, and screening for self-harm.
  • Registered dietitian — the structured meal plan that stops the restrict-binge cycle, and reintroducing "forbidden" foods.
  • Therapist — CBT-E, trigger identification, impulse and emotion regulation skills.
  • Dentist — enamel protection, fluoride, restoration. Refer early.
  • Psychiatrist — fluoxetine, and the comorbid depression, substance use, self-harm, and borderline traits that are common here.
5 · How can it get worse / be prevented?
  • 🚨 Fatal arrhythmia from hypokalemia — the leading medical cause of death. Also cardiomyopathy from ipecac abuse, which is cumulative and irreversible.
  • 🚨 Mallory-Weiss tear or esophageal rupture from forceful vomiting — hematemesis is an emergency. Aspiration pneumonia from vomiting is also a risk.
  • ⚠️ Cathartic colon from chronic laxative abuse — the bowel stops working without stimulation, so stopping laxatives causes severe constipation and rebound edema. Teach them this in advance or they will restart the laxatives.
  • ⚠️ Permanent dental destruction, chronic esophagitis, gastric rupture (rare, from massive binges), electrolyte-driven muscle weakness, and menstrual irregularity.
  • ✅ Teach: do not brush immediately after vomiting — the enamel is acid-softened and brushing scrubs it off; rinse with water or a bicarbonate rinse first and wait about 30 minutes. Use fluoride and see the dentist.
  • ✅ Teach: stop dieting and restricting — that is what starts the binge; eat on a schedule; identify triggers and use a planned alternative (call someone, leave the kitchen, go outside for 10 minutes); expect fluid retention and constipation for 1–2 weeks after stopping laxatives and diuretics; report palpitations, dizziness, or fainting immediately; and keep the follow-up appointments because relapse is common.
⭐ If you only remember one thing: Check the potassium — hypokalemia is the killer, and vomiting gives metabolic alkalosis while laxatives give metabolic acidosis. Fluoxetine 60 mg is the only approved drug; bupropion is contraindicated. Look for Russell's sign, eroded enamel, and swollen parotids in a normal-weight patient.

🥃 Alcohol Withdrawal

One-line hook: this is the withdrawal that can kill — alcohol and benzodiazepine withdrawal are the two lethal ones; opioid withdrawal is miserable but survivable. Know the clock: tremors at 6–12 hours, seizures at 24–48, delirium tremens at 48–96.

1 · What is happening in the body?
  • Alcohol enhances GABA (the brake) and suppresses glutamate (the accelerator). With chronic use the brain compensates by down-regulating GABA receptors and up-regulating glutamate/NMDA receptors.
  • Remove the alcohol and you are left with a brain that has almost no brake and a floored accelerator — that unopposed excitation is the tremor, the tachycardia, the hypertension, the hallucinations, and the seizures. Every symptom follows from that one sentence.
  • Massive sympathetic outflow → tachycardia, hypertension, diaphoresis, fever, and dilated pupils.
  • Thiamine (B1) deficiency from poor intake and impaired absorption → Wernicke encephalopathy, which becomes irreversible Korsakoff psychosis if untreated. Also common: folate, magnesium, and phosphorus depletion.
  • Benzodiazepines work because they are cross-tolerant with alcohol — they substitute at the same GABA receptor and let you taper the brain down instead of dropping it off a cliff.
  • Risk of severe withdrawal is highest in patients with a prior history of withdrawal seizures or DTs (kindling), heavy daily intake, and concurrent medical illness.
2 · How do you know?
  • ⏱️ THE TIMELINE — memorize it:
    • 6–12 hours — minor withdrawal: tremors (hands, tongue), anxiety, nausea, insomnia, headache, diaphoresis, tachycardia and hypertension. Patient is oriented.
    • 12–24 hours — alcoholic hallucinosis: visual, tactile, or auditory hallucinations (classically bugs or insects) with intact orientation and stable vital signs. This is NOT delirium tremens — that distinction is a test question.
    • 24–48 hours — withdrawal seizures: generalized tonic-clonic, usually brief and self-limited, often in a short cluster. Peak risk right around 24 hours.
    • 48–96 hours (up to 5 days) — DELIRIUM TREMENS: the emergency.
  • 🚨 Delirium tremens = clouded sensorium + everything else. Disorientation and fluctuating confusion, severe agitation, vivid hallucinations, gross tremor, fever, drenching diaphoresis, heart rate over 120, hypertension. The distinguishing feature of DTs is the altered level of consciousness — hallucinosis keeps orientation, DTs loses it. Untreated mortality is significant.
  • 🧪 CIWA-Ar is the scoring tool (nausea, tremor, sweats, anxiety, agitation, tactile/auditory/visual disturbance, headache, orientation). Score under 8 = minimal · 8–15 = moderate, medicate · over 15 = severe, high DT risk. Score on a schedule and medicate to the score.
  • Wernicke encephalopathy triad: confusion + ataxia + ophthalmoplegia/nystagmus. If it progresses to Korsakoff, you get permanent short-term memory loss with confabulation (filling gaps with invented detail, not lying).
  • 📈 Deterioration: rising CIWA despite dosing, temperature over 101°F, heart rate over 120, new disorientation, or a seizure — escalate to a higher level of care.
3 · How do you fix it?
  • 💊 Benzodiazepines are the treatment — chlordiazepoxide, diazepam, or lorazepam, dosed symptom-triggered to the CIWA score (better outcomes and less total drug than fixed scheduling). Use lorazepam in liver disease, older adults, or a patient with delirium — it has no active metabolites and is not oxidized by the liver.
  • 💊 Thiamine 100 mg — and give it BEFORE or with any glucose. Never give IV dextrose or a carbohydrate load to an alcohol-dependent patient before thiamine — the glucose consumes the last of the thiamine and can precipitate Wernicke encephalopathy. Then add folate, a multivitamin, and magnesium.
  • Environment: quiet, well-lit room (shadows feed hallucinations), minimal stimulation, familiar staff, frequent reorientation, and a clock and calendar in view. Do not confront or argue with the hallucinations; state reality calmly and reassure.
  • Safety: seizure precautions (bed low, rails padded, suction and oxygen at bedside), fall precautions, continuous or frequent monitoring, and restraints only as a last resort because they increase agitation and injury.
  • 💧 Fluid and electrolyte replacement — these patients are dehydrated and depleted; correct magnesium, potassium, and phosphorus. Monitor vital signs and glucose frequently. Adjuncts: phenobarbital or propofol for refractory DTs, and clonidine or beta blockers for autonomic symptoms only (they do not prevent seizures — do not use them alone).
  • 💊 Long-term relapse prevention: disulfiram (causes flushing, throbbing headache, vomiting, tachycardia, and hypotension if alcohol is consumed — avoid all hidden alcohol: mouthwash, cough syrup, aftershave, vanilla extract, sauces; effect lasts up to 14 days after the last dose) · naltrexone (reduces craving and reward; contraindicated with opioids and in acute hepatitis) · acamprosate (reduces post-acute craving; renally cleared).
4 · Who is involved?
  • Nurse — the CIWA scores, the symptom-triggered dosing, the vital sign trend, the seizure precautions, and the reorientation. Withdrawal is a nursing-assessment-driven diagnosis.
  • Provider / hospitalist / intensivist — the protocol, escalation to ICU for DTs, and managing the co-occurring pancreatitis, GI bleed, cirrhosis, and cardiomyopathy.
  • Pharmacist — benzodiazepine selection for liver function, thiamine timing, disulfiram and naltrexone counseling.
  • Addiction medicine / substance use counselor — detox is not treatment; the counselor arranges what happens after.
  • Social worker — rehab placement, insurance, housing, transportation, and family issues.
  • AA / peer recovery and family (Al-Anon) — long-term abstinence support and the household changes that make it possible.
5 · How can it get worse / be prevented?
  • 🚨 Delirium tremens — hyperthermia, arrhythmia, cardiovascular collapse, aspiration, injury during agitation, and death. Prevented almost entirely by early, adequate benzodiazepine dosing, which is why undermedicating is the dangerous error.
  • 🚨 Status epilepticus from repeated withdrawal seizures, and Korsakoff psychosis from delayed thiamine — both are permanent injuries caused by preventable delays.
  • ⚠️ Kindling: each withdrawal episode makes the next one more severe and lowers the seizure threshold. A patient with a prior DT history is high risk from the first hour.
  • ⚠️ Concurrent medical crises that mimic or mask withdrawal: head injury, subdural hematoma, hypoglycemia, infection, GI bleed, hepatic encephalopathy. Do not assume every confused alcohol-dependent patient is only withdrawing.
  • ✅ Teach the patient: do not stop drinking abruptly on your own after heavy daily use — medically supervised withdrawal is safer; take thiamine and the vitamins; expect sleep disturbance and cravings for weeks; and on disulfiram, read every label for alcohol.
  • ✅ Teach family: withdrawal peaks in the first 2–4 days and needs medical supervision; recognize confusion, fever, and severe tremor as reasons to call; support the aftercare plan; and Al-Anon exists for them, not just the patient.
⭐ If you only remember one thing: 6–12 h tremors · 12–24 h hallucinations with intact orientation · 24–48 h seizures · 48–96 h delirium tremens. Treat with benzodiazepines dosed to the CIWA score, and give thiamine before any glucose.

💉 Opioid Withdrawal & Overdose

One-line hook: overdose kills, withdrawal does not — overdose is pinpoint pupils and a stopped respiratory drive; withdrawal is dilated pupils, runny everything, and cramping. Look at the pupils and the respiratory rate and you have the answer.

1 · What is happening in the body?
  • Opioids bind mu receptors → analgesia, euphoria, sedation, suppressed brainstem respiratory drive, pupillary constriction, cough suppression, and slowed GI motility.
  • Overdose is respiratory: the brainstem stops responding to rising CO₂, breathing slows and stops, and the patient dies of hypoxia — not of the sedation itself. That is why respiratory rate is the number you watch.
  • Chronic use suppresses the locus coeruleus (the noradrenergic center). Remove the opioid and norepinephrine rebounds massively — which is exactly the withdrawal picture: sweating, gooseflesh, cramping, diarrhea, yawning, lacrimation, and dilated pupils.
  • Tolerance falls fast during abstinence. The highest-risk moment for fatal overdose is relapse after a period of abstinence — after jail, detox, or hospitalization — because the patient takes their old dose with a new, low tolerance.
  • Naloxone lasts 30–90 minutes; most opioids last far longer — especially methadone, extended-release formulations, and fentanyl analogs. This is why re-sedation after a good response is a real and lethal event.
  • Neonatal abstinence syndrome: in-utero exposure produces withdrawal in the newborn (high-pitched cry, irritability, tremors, poor feeding, diarrhea) — scored with the Finnegan tool.
2 · How do you know?
  • 🚨 OVERDOSE — the classic triad: pinpoint (miotic) pupils · respiratory depression (rate under 12, shallow, or apneic) · decreased level of consciousness. Plus bradycardia, hypotension, cyanosis, cold clammy skin, and absent bowel sounds. The respiratory rate is the priority assessment.
  • 🚨 Late overdose findings: non-cardiogenic pulmonary edema (frothy sputum, crackles), aspiration, seizures (meperidine, tramadol), and anoxic brain injury.
  • WITHDRAWAL — the opposite picture, everything running: dilated pupils (mydriasis), yawning, lacrimation, rhinorrhea, piloerection ("cold turkey"), diaphoresis, chills alternating with flushing, muscle and bone aches, abdominal cramping, nausea, vomiting, diarrhea, restlessness, insomnia, anxiety, and intense craving.
  • 🧪 COWS (Clinical Opiate Withdrawal Scale) scores severity and determines when it is safe to induct buprenorphine. Urine drug screen; note that fentanyl and many synthetics do not show on a standard opiate screen.
  • ⏱️ Onset: 6–12 hours after a short-acting opioid (heroin, oxycodone), peaking at 36–72 hours and resolving in about 5–7 days; 24–48 hours after methadone, lasting up to 2–3 weeks.
  • 📈 Deterioration in withdrawal: it is dehydration and electrolyte loss from vomiting and diarrhea that hurts people — plus the risk that intolerable symptoms drive them to leave and use at their old dose.
3 · How do you fix it?
  • 🚨 Overdose — airway first, then naloxone. Open the airway, ventilate with bag-valve-mask and oxygen, then give naloxone 0.4–2 mg IV, IM, SC, or intranasal, repeated every 2–3 minutes until the patient is breathing adequately. The goal is a respiratory rate over 10, not a fully awake patient — waking them completely dumps them into violent withdrawal.
  • After naloxone: keep monitoring for at least 2 hours, and much longer for long-acting opioids. Never discharge a patient who responded to naloxone without an observation period — the naloxone wears off before the opioid does and they can stop breathing again. A continuous infusion may be required. Naloxone will also precipitate acute withdrawal in a dependent patient — expect vomiting and agitation, and protect the airway.
  • 💊 Withdrawal — medication-assisted treatment (MAT) is the standard of care. Methadone (full agonist; dispensed through a licensed opioid treatment program; monitor for QT prolongation and sedation) · Buprenorphine/naloxone (partial agonist with a ceiling on respiratory depression; the patient must already be in moderate withdrawal (COWS) before the first dose or it precipitates withdrawal) · Naltrexone (full antagonist for relapse prevention; requires 7–10 days opioid-free first, and it raises overdose risk if the patient relapses).
  • 💊 Symptom control: clonidine for the autonomic storm (sweating, cramping, anxiety — monitor blood pressure and hold for hypotension), loperamide for diarrhea, ondansetron for nausea, dicyclomine for cramps, NSAIDs for aches, hydroxyzine or trazodone for sleep, and IV or oral fluids and electrolytes.
  • Nursing approach: non-judgmental, matter-of-fact, and consistent. Assess and treat real pain — having a substance use disorder does not remove the right to analgesia, though the plan needs to be explicit. Set clear limits about visitors and belongings, and monitor for diverted substances.
  • ✅ Harm reduction is nursing care: prescribe and teach take-home naloxone to the patient and to the family, teach not to use alone, warn about fentanyl contamination, provide fentanyl test strips and syringe services where available, and connect to MAT before discharge.
4 · Who is involved?
  • EMS and emergency nurses — airway, naloxone, and the observation window.
  • Addiction medicine provider — MAT induction, buprenorphine timing, methadone program referral.
  • Nurse — COWS scoring, respiratory monitoring after naloxone, hydration, symptom relief, naloxone teaching, and treating the patient without contempt (stigma is the reason people do not come back).
  • Pharmacist — naloxone dispensing and demonstration, MAT interactions, methadone QT monitoring.
  • Social worker / case manager — treatment placement, insurance, housing, custody and legal issues, transportation to the daily methadone dose.
  • Peer recovery specialist and family — naloxone in the home, recognizing overdose, calling 911, and Good Samaritan law protections.
5 · How can it get worse / be prevented?
  • 🚨 Re-sedation after naloxone wears off — the classic preventable death. Long-acting opioids outlast the antidote.
  • 🚨 Fatal overdose on relapse after abstinence — lost tolerance plus the old dose. Every discharge from detox, jail, or the hospital is a high-risk moment; naloxone goes home with them.
  • 🚨 Fentanyl and its analogs in the illicit supply — far more potent, unpredictably dosed, and often require repeated or higher naloxone doses.
  • ⚠️ Injection-related complications: endocarditis, osteomyelitis, cellulitis and abscess, HIV and hepatitis B and C, sepsis. Also constipation and bowel obstruction with chronic use, and respiratory arrest when opioids are combined with benzodiazepines or alcohol.
  • ⚠️ Withdrawal itself is not usually fatal in adults, but it is dangerous in pregnancy — untreated maternal withdrawal risks fetal distress and preterm labor, so pregnant patients are maintained on methadone or buprenorphine, not detoxed.
  • ✅ Teach: keep naloxone where others can find it and show them how to use it; do not use alone; do not mix with alcohol or benzodiazepines; your tolerance drops after even a few days off; take the MAT daily as prescribed and do not stop because you feel fine; and store all opioids locked, then dispose of leftovers at a take-back site.
⭐ If you only remember one thing: Overdose = pinpoint pupils + respiratory depression + decreased LOC → airway, ventilate, naloxone, then WATCH, because naloxone wears off first. Withdrawal = dilated pupils and everything running — awful, not lethal. The deadliest moment of all is relapse after abstinence.

🚨 Suicidal Ideation & Safety

One-line hook: ask directly, in plain words, every time — asking does not plant the idea, and the answer decides everything else you do. A patient with a plan, the means, and a lethal method is not a "watch closely" patient; they are a 1:1.

1 · What is happening in the body?
  • Low serotonin turnover and impaired prefrontal impulse control — the classic finding in completed suicide. Impulsivity plus hopelessness is the lethal combination, not sadness alone.
  • Hopelessness predicts suicide better than the severity of depression does. Assess hopelessness specifically: "what do you think the next few months look like?"
  • Constricted thinking — the patient literally cannot generate alternatives; suicide appears as the only remaining option. This is why problem-solving and connection interrupt it.
  • Substances remove the last brake: alcohol and stimulant intoxication account for a large share of impulsive attempts.
  • Suicidal crises are usually time-limited. The whole logic of means restriction rests on this — if the method is not within reach during the acute window, most people survive it and most survivors do not go on to die by suicide.
  • Elevated risk populations: prior attempt (the single strongest predictor), older white men, adolescents and young adults, veterans, LGBTQ+ youth, people with chronic pain or terminal illness, health care workers, and anyone recently discharged from a psychiatric unit.
2 · How do you know?
  • Ask directly and unambiguously: "Are you thinking about killing yourself?" — not "you're not thinking of doing anything silly, are you?" Then follow up: Do you have a plan? What is the plan? Do you have access to it (the gun, the pills)? Have you set a time? Have you tried before?
  • Risk rises with each yes: ideation → plan → means available → specific method that is highly lethal (firearm, hanging) → a set time → prior attempt. Also assess intent, rehearsal behavior, and the absence of protective factors.
  • 🧪 Tools: Columbia Suicide Severity Rating Scale (C-SSRS) — the standard; ASQ for screening; SAD PERSONS as a memory aid for risk factors (Sex male, Age, Depression, Previous attempt, Ethanol, Rational thinking loss, Social supports lacking, Organized plan, No spouse, Sickness).
  • 🚩 Warning signs you must act on: giving away prized possessions, making a will or "getting affairs in order," saying goodbye, writing notes, buying a weapon or hoarding medication, sudden withdrawal — and a sudden unexplained calm or lift in mood after a period of severe depression, which often means the decision has been made.
  • ⏱️ The two high-risk windows: 1–2 weeks after starting an antidepressant (energy returns before mood does) and the days to weeks immediately after discharge from a psychiatric hospitalization.
  • Protective factors matter and should be documented: children at home, religious prohibition, a strong therapeutic relationship, future plans, responsibility for pets, and reasons for living the patient can name.
3 · How do you fix it?
  • Safety is the priority above all other nursing diagnoses. Match observation to risk: 1:1 continuous observation within arm's length (including in the bathroom and while sleeping) for active ideation with a plan and intent; 15-minute checks at irregular, unpredictable intervals for lower acuity — fixed-schedule checks are predictable and can be timed around. Document every check by hand at the time it happens.
  • Means restriction — the intervention with the best evidence. Remove belts, shoelaces, drawstrings, scarves, cords and phone chargers, sharps and razors, glass, mirrors, plastic bags, lighters, and all medications. Search belongings and anything brought by visitors. Use breakaway rods and non-weight-bearing fixtures. At home: lock up or remove firearms and store ammunition separately, lock medications, and dispose of extras. Prescribe only limited quantities.
  • 💊 Watch for cheeking and hoarding — check the mouth, use liquid or dissolving forms, and account for every dose. Also monitor food and fluid intake, and remain alert during shift change and mealtimes, when staffing attention dips.
  • Build a collaborative safety plan (not a "no-suicide contract"): personal warning signs → internal coping strategies → people and places that distract → people to call → professionals and crisis line (988) → means restriction steps. Never rely on a "no-harm contract" or a patient's promise as your safety intervention — there is no evidence it prevents suicide, and it can never replace observation and means restriction.
  • 💬 Therapeutic communication — say this: use open-ended questions, silence, offering self ("I'll sit with you"), reflection ("you sound hopeless"), clarification ("tell me what you mean by 'done'"), making observations ("I notice you haven't eaten"), and focusing. Stay calm and non-judgmental; take every statement seriously.
  • 💬 Do NOT say this — these sound kind and are not therapeutic: false reassurance ("everything will be fine," "don't worry") · minimizing ("you have so much to live for," "others have it worse") · giving advice ("what you should do is...") · "why" questions ("why would you do that?" — they demand a justification and put the patient on the defensive) · approval or disapproval ("good, that's the right attitude") · changing the subject · defending the staff or the family · challenging or arguing · promising to keep a secret. Never promise to keep suicidal statements confidential — tell the patient plainly that you must share this with the team to keep them safe.
4 · Who is involved?
  • Nurse — the risk assessment at every contact, the observation level, environmental safety, medication accounting, and the documented handoff. You are the person physically standing between the patient and the method.
  • Psychiatrist / provider — the level of care decision, the observation order, treatment of the underlying illness, and involuntary hold paperwork when the patient will not stay voluntarily.
  • Entire unit staff, including techs, housekeeping, and dietary — safety is everyone's job; plastic bags, silverware, and cleaning chemicals arrive with these staff.
  • Therapist — CBT for suicide prevention, DBT, and safety planning intervention with follow-up contacts.
  • Family and support system — they carry out means restriction at home and are the ones who notice the warning signs. Involve them with the patient's knowledge, and give them the crisis line.
  • Case manager — the post-discharge follow-up call and appointment within days, because the post-discharge window is a peak-risk period.
5 · How can it get worse / be prevented?
  • 🚨 Attempt on the unit — the failure points are almost always the same: an unsearched belonging, an unobserved bathroom, a predictable check schedule, a hoarded medication, or a break in communication at handoff.
  • 🚨 The energy window on antidepressants and the post-discharge period — increase support at exactly the moment it usually decreases.
  • ⚠️ Contagion — a suicide or attempt on a unit, in a school, or in a community raises risk for others. Debrief the milieu, screen exposed peers, and follow safe-messaging guidelines (no method detail, no glamorizing).
  • ⚠️ Alcohol and substance use, access to firearms, a recent loss or humiliation (job, relationship, legal charge), and untreated pain all sharply raise near-term risk.
  • ✅ Teach patient and family: remove the means from the home before discharge, not after; keep the safety plan physically accessible; use 988 or go to the ED for a crisis; go to the follow-up appointment within a week; no alcohol; and take suicidal talk seriously every single time, even if it has been said before.
  • ✅ Teach staff and family the truth about myths: asking about suicide does not cause it, people who talk about it do attempt it, and improvement in mood does not mean the risk is over.
⭐ If you only remember one thing: Ask directly — "Are you thinking of killing yourself?" — then assess plan, means, and lethality, and restrict the means. 1:1 arm's-length observation for an active plan; irregular 15-minute checks otherwise. A no-harm contract is never a safety intervention, and the highest-risk moment is when the patient suddenly seems better.

🕰️ Delirium vs Dementia

One-line hook: delirium is sudden, fluctuating, and reversible; dementia is slow, steady, and permanent. If confusion appeared over hours to days, it is delirium until you have ruled out a cause — go looking for infection, drugs, hypoxia, and electrolytes.

1 · What is happening in the body?
  • Delirium = acute global brain dysfunction from a systemic insult. Neurotransmitter chaos (too little acetylcholine, too much dopamine) plus inflammatory cytokines disrupt attention and consciousness. The brain itself is structurally fine — it is being poisoned, starved, or inflamed.
  • Delirium causes — DELIRIUM / think "what changed?": infection (UTI and pneumonia are the classics in older adults), medications (anticholinergics, benzodiazepines, opioids, antihistamines, steroids), hypoxia, dehydration, electrolyte and glucose abnormalities, uncontrolled pain, urinary retention or constipation, alcohol or benzodiazepine withdrawal, post-operative state, and sleep deprivation or sensory deprivation.
  • Dementia = progressive structural neuron loss. Alzheimer (amyloid plaques and tau tangles, starting in the hippocampus — which is why short-term memory goes first) · vascular (stepwise decline after infarcts) · Lewy body (alpha-synuclein — visual hallucinations, parkinsonism, fluctuating cognition, severe antipsychotic sensitivity) · frontotemporal (personality and behavior change before memory).
  • They coexist constantly. Dementia is the single biggest risk factor for delirium, and delirium superimposed on dementia is the usual hospital picture. A dementia patient who is suddenly much worse has delirium.
  • Sundowning — increased confusion and agitation in the late afternoon and evening — occurs in both, driven by fatigue, low light, and disrupted circadian rhythm.
  • Delirium is independently associated with longer stays, functional decline, institutionalization, and higher mortality — it is not a benign nuisance.
2 · How do you know?
  • ⭐ SIDE BY SIDE — the comparison they test:
    • Onset — Delirium: abrupt, hours to days, and you can often name the day. Dementia: insidious, months to years, family cannot say when it started.
    • Course — Delirium: fluctuates within the same day, lucid one hour and confused the next. Dementia: slowly progressive and relatively stable day to day.
    • Attention / level of consciousness — Delirium: impaired — this is the hallmark; distractible, cannot sustain focus, clouded or altered LOC. Dementia: alert and attentive until the late stages.
    • Duration — Delirium: hours to days, usually under a month. Dementia: years, until death.
    • Reversibility — Delirium: reversible if you find and fix the cause. Dementia: irreversible and progressive (a few causes such as B12 deficiency, hypothyroidism, and normal pressure hydrocephalus are treatable — always screen for them).
    • Perception — Delirium: hallucinations common, usually visual, plus illusions and misperceptions; often frightening. Dementia: hallucinations uncommon until late (except Lewy body, where vivid visual hallucinations come early).
    • Psychomotor — Delirium: hyperactive (agitated, pulling lines), hypoactive (quiet, withdrawn, sleepy — the most commonly missed and the most deadly), or mixed. Dementia: usually normal early; wandering and apraxia later.
    • Speech / thought — Delirium: incoherent, rambling, disorganized. Dementia: word-finding difficulty and empty speech, progressing to aphasia.
    • Sleep-wake cycle — Delirium: grossly disrupted, often reversed. Dementia: fragmented, with sundowning.
    • Memory — Delirium: recent memory impaired because attention is impaired. Dementia: recent memory lost first, remote memory preserved longest.
  • 🧪 Tools: CAM (Confusion Assessment Method) — positive requires acute onset with fluctuating course AND inattention, plus either disorganized thinking or altered LOC. Use CAM-ICU in critical care. For dementia: MMSE or MoCA, plus a functional assessment.
  • 🧪 Delirium workup: urinalysis and culture, CBC, electrolytes, glucose, BUN/creatinine, calcium, liver and thyroid function, oxygen saturation, medication review, bladder scan, and a head CT if there was a fall or focal deficit.
  • 📈 The most important assessment is the baseline. Always ask the family "is this how they normally are?" — without a baseline you cannot tell chronic from acute, and hypoactive delirium in a dementia patient will be missed entirely.
3 · How do you fix it?
  • 🚨 Delirium: find and treat the cause. That is the treatment. Culture and treat the infection, correct the sodium and glucose, oxygenate, hydrate, relieve the pain, scan the bladder and disimpact the bowel, and stop the offending drug. Sedating a delirious patient without finding the cause treats your discomfort, not theirs.
  • Non-pharmacologic measures first, for both conditions: reorient frequently, keep a clock and calendar visible, put the glasses and hearing aids back on (sensory deprivation alone causes delirium), open the blinds by day and reduce noise at night to restore the sleep-wake cycle, keep the same staff, place familiar objects and photos at the bedside, mobilize early, and get family to stay.
  • 💊 Medication is a last resort for danger, not for wandering or calling out. Low-dose haloperidol or an atypical antipsychotic only when the patient is a danger to self or others. Never give benzodiazepines for delirium — they make it worse — except when the delirium is caused by alcohol or benzodiazepine withdrawal, where benzodiazepines are the treatment. And never give antipsychotics to a patient with Lewy body dementia; they cause severe, sometimes fatal sensitivity reactions.
  • Restraints make delirium worse — they increase agitation, injury, deconditioning, and death. Use sitters, family presence, low beds, bed and chair alarms, and camouflaged exits instead. If restraints are unavoidable, all the seclusion-and-restraint rules apply: provider order, no PRN orders, continuous observation, checks every 15 minutes, and toileting, fluids, and range of motion every 2 hours.
  • 💊 Dementia medications slow decline; they do not reverse it. Cholinesterase inhibitors (donepezil, rivastigmine, galantamine) for mild-to-moderate disease — GI upset, bradycardia, and syncope are the side effects; memantine (NMDA antagonist) for moderate-to-severe, and it can be combined. Treat depression, which is common and can look like worsening dementia.
  • Communicating with a dementia patient: approach from the front, make eye contact, use their name, one simple direction at a time, allow extra time to respond, use short concrete words and gestures, do not quiz or argue about facts, redirect and validate the feeling instead of correcting the delusion, and keep the routine identical every day. Break tasks into single steps and lay clothing out in order.
4 · Who is involved?
  • Nurse — the person who detects delirium, because you have the baseline, the trend, and the night shift. Screen with CAM every shift in at-risk patients.
  • Provider / geriatrician — the workup, the deprescribing (Beers criteria for potentially inappropriate medications in older adults), and the dementia diagnosis.
  • Pharmacist — anticholinergic burden review, which is often the single highest-yield intervention for delirium.
  • Physical and occupational therapy — early mobilization prevents delirium; home safety evaluation for dementia (locks, stove shutoffs, removing rugs, hot water temperature).
  • Social worker and case manager — placement, respite care, adult day programs, and financial and legal planning (advance directives and power of attorney while the patient still has capacity).
  • Family caregiver — the treatment plan depends on them, and caregiver burnout is a clinical problem you must assess for. Refer to the Alzheimer's Association, support groups, and respite services.
5 · How can it get worse / be prevented?
  • 🚨 Missed hypoactive delirium — the quiet, withdrawn, "pleasantly confused" patient who is actually septic or hypoxic. It has the worst outcomes precisely because nobody investigates a patient who is not causing trouble.
  • 🚨 Complications of both: falls and hip fracture, aspiration pneumonia, dehydration and malnutrition, pressure injuries, wandering and elopement, and death. Aspiration pneumonia is the most common cause of death in advanced dementia.
  • ⚠️ Every delirium episode accelerates long-term cognitive decline and raises the risk of permanent functional loss and nursing home placement. Prevention is worth more than treatment.
  • ⚠️ Prevention bundle (HELP-style) — this is highly testable: reorientation, early mobilization, sleep protection (cluster care, no vitals at 3 a.m. if avoidable, no caffeine at night), hydration and nutrition, glasses and hearing aids, pain control, bowel and bladder management, and minimizing anticholinergics, benzodiazepines, and Foley catheters.
  • ✅ Teach the family in dementia: keep routines and the environment unchanged, simplify choices, label rooms and drawers, install door alarms and enroll in a wandering-safe-return program, use an ID bracelet, remove stove knobs and car keys when driving is no longer safe, expect and do not argue with repetitive questions, and plan for the next stage before it arrives.
  • ✅ Teach the family in delirium: this is usually temporary and has a cause; bring in glasses, hearing aids, and familiar objects; stay and reorient; and report any sudden change in alertness immediately — the family's "he isn't himself" is often the earliest and most accurate finding you will get.
⭐ If you only remember one thing: Sudden + fluctuating + inattentive = DELIRIUM → find the cause (infection, drugs, hypoxia, electrolytes, retention, withdrawal). Slow + steady + alert-until-late = DEMENTIA. Delirium is reversible, dementia is not, and a dementia patient who suddenly gets worse has delirium on top. No benzodiazepines for delirium (unless it is alcohol withdrawal), and no antipsychotics in Lewy body.

🎯 ADHD

One-line hook: an executive function and self-regulation disorder, not a motivation problem — symptoms must appear before age 12, in two or more settings. Trouble only at school and never at home is something else.

1 · What is happening in the body?
  • Underactive dopamine and norepinephrine signaling in the prefrontal cortex — the region that runs attention, inhibition, working memory, and planning. It is under-aroused, not over-aroused.
  • That is the whole paradox of stimulants: methylphenidate and amphetamines raise dopamine and norepinephrine in the prefrontal cortex, which turns the brakes back on. They calm the patient because they stimulate the inhibitory system.
  • Delayed maturation of the prefrontal cortex — the brain gets there, just years late, which is why symptoms often soften in adulthood but rarely disappear entirely.
  • Highly heritable — if one parent has it, look for it in the other family members; the parent is often undiagnosed themselves.
  • Three presentations: predominantly inattentive (quiet, daydreaming, often girls, most often missed), predominantly hyperactive-impulsive, and combined.
  • Criteria: 6 or more symptoms (5 if 17 or older) for at least 6 months, onset before age 12, present in 2+ settings, with clear functional impairment.
2 · How do you know?
  • Inattention: careless mistakes, cannot sustain attention, does not seem to listen, does not finish tasks, poor organization, avoids sustained mental effort, loses things constantly, easily distracted, forgetful in daily activities.
  • Hyperactivity/impulsivity: fidgets, leaves seat, runs or climbs inappropriately, cannot play quietly, "driven by a motor," talks excessively, blurts out answers, cannot wait a turn, interrupts and intrudes.
  • 🧪 Assessment: collateral rating scales from both parents and teachers (Vanderbilt, Conners) — this is how you establish the "two settings" criterion. Plus a developmental history, school records, and a full physical.
  • Rule out the mimics before diagnosing: hearing or vision impairment, sleep apnea or chronic sleep deprivation, learning disability, absence seizures, lead exposure, thyroid disease, anxiety, depression, trauma/PTSD, and autism.
  • Before and during stimulant treatment, assess: baseline height, weight, blood pressure, heart rate, and a cardiac and family sudden-death history; also screen for tics and for substance use or diversion risk in the household.
  • 📈 Deterioration signs: school failure and repeated suspensions, peer rejection, injuries from impulsivity, escalating family conflict, and emerging oppositional defiant disorder, conduct disorder, depression, or substance use — ADHD rarely travels alone.
3 · How do you fix it?
  • 💊 Stimulants are first line and highly effective. Methylphenidate (Ritalin, Concerta, Daytrana patch) and amphetamine salts (Adderall, Vyvanse, dextroamphetamine). Schedule II — no refills, requires a new prescription each time.
  • ⏰ Stimulant timing rules — heavily tested: give after breakfast and give the last dose before 4 p.m. to prevent insomnia. Give after meals, not before, because appetite suppression is the most common side effect — then offer a high-calorie, high-protein snack in the evening when the drug wears off and hunger returns.
  • 💊 Stimulant monitoring: plot height and weight on a growth chart at every visit — growth suppression is a real effect; check blood pressure and heart rate; watch for insomnia, headache, irritability or rebound in the late afternoon, tics, and (rarely) psychosis. Drug holidays on weekends or over the summer may be used to allow catch-up growth. Never give a stimulant to a patient taking an MAOI or within 14 days of one — hypertensive crisis. Store locked; these are among the most diverted drugs in schools.
  • 💊 Non-stimulants for tics, substance-use risk, or intolerable side effects: atomoxetine (an NRI — takes 4–6 weeks, is not a controlled substance, carries a black box warning for suicidal ideation in children and adolescents, and can cause hepatotoxicity — teach reporting of jaundice, dark urine, or right upper quadrant pain) · guanfacine ER and clonidine ER (alpha-2 agonists — sedation and hypotension; monitor blood pressure and do not stop abruptly, which causes rebound hypertension; useful when hyperactivity and sleep are the problem).
  • Behavioral management is the other half, and it is first-line before medication in preschoolers: parent behavior training, consistent daily routine and structure, immediate and specific praise, a token or point system with immediate rewards, one instruction at a time with eye contact and repeat-back, short work periods with movement breaks, and a low-distraction workspace.
  • 🏫 School accommodations: a 504 plan or IEP — preferential seating near the teacher and away from windows and doors, extended time on tests, testing in a separate quiet room, written and verbal instructions, an assignment notebook checked daily, and permitted movement.
4 · Who is involved?
  • Pediatrician / psychiatric provider — diagnosis, medication trials and titration, growth and cardiac monitoring.
  • Parents / caregivers — the primary implementers; parent behavior training changes outcomes as much as medication does. They also control storage and administration of a controlled substance.
  • Teachers and school nurse — rating scales, the 504/IEP, in-school dosing, and observing the response.
  • School psychologist — testing for the co-occurring learning disabilities that are present in a large share of these children.
  • Therapist — behavioral therapy, social skills, organizational coaching, and treating comorbid anxiety or depression.
  • Pharmacist — Schedule II refill rules, MAOI interaction, timing counseling, and diversion prevention.
5 · How can it get worse / be prevented?
  • 🚨 Stimulant misuse and diversion — selling or sharing pills, snorting, or using to stay awake. Count pills, store locked, and use extended-release or prodrug (lisdexamfetamine) forms where risk is high.
  • 🚨 Stimulant adverse effects to act on: chest pain, palpitations, syncope, marked hypertension, new tics, hallucinations, or growth falling off the curve. Cardiac events are rare but structural heart disease should be excluded.
  • ⚠️ Untreated ADHD carries real consequences: academic failure, injuries and motor vehicle crashes, early substance use, unplanned pregnancy, job instability, and low self-esteem from years of being called lazy or bad. Treated ADHD lowers, not raises, later substance use risk.
  • ⚠️ Rebound in the late afternoon as the drug wears off (irritability, tearfulness, a burst of hyperactivity) — this is expected and can be managed with dosing changes; do not mistake it for worsening disease.
  • ✅ Teach the family: medication does not cure ADHD, it makes the behavioral strategies work; keep the routine identical; use visual schedules, timers, and checklists; break tasks into single steps; praise effort immediately and specifically; and preserve self-esteem — find something the child is good at and protect it.
  • ✅ Teach: give the last dose before 4 p.m., give with or after food, offer an evening snack, report chest pain or fainting, do not stop clonidine or guanfacine abruptly, and keep every growth and blood pressure check.
⭐ If you only remember one thing: Stimulants: give after meals, last dose before 4 p.m., and monitor height, weight, heart rate, and blood pressure. Symptoms must start before age 12 in 2+ settings, and structure plus behavioral management is half the treatment.

🧩 Autism Spectrum Disorder

One-line hook: two required features — persistent deficits in social communication AND restricted, repetitive behaviors — present from early development. Nursing care is about routine, sensory load, and literal language, not about changing who the child is.

1 · What is happening in the body?
  • Atypical brain connectivity and synaptic pruning — over-connection locally and under-connection between distant regions. That pattern explains the combination of intense narrow focus with difficulty integrating social context.
  • Differences in the social brain network (amygdala, fusiform face area, mirror neuron systems) → reduced automatic reading of faces, tone, and intent. Social cues that are effortless for others must be consciously decoded.
  • Sensory processing differences — over- or under-responsiveness to sound, light, touch, texture, and smell. This is not a preference; ordinary hospital noise and lighting can be physically painful and is a common cause of meltdowns.
  • Strongly genetic and neurodevelopmental, with onset in the early developmental period even if it is not recognized until demands increase.
  • Vaccines do not cause autism — the original claim was fraudulent and retracted, and has been disproven repeatedly in very large studies. Say this clearly and without judgment when a parent asks.
  • Frequently co-occurring: intellectual disability (in some, not all), epilepsy, ADHD, anxiety, GI problems, sleep disorders, and feeding selectivity.
2 · How do you know?
  • Social communication deficits: poor or absent eye contact, does not respond to their name, no joint attention (does not point at things to share interest or follow a point), reduced social reciprocity, difficulty with back-and-forth conversation, trouble with nonverbal cues and facial expression, difficulty making and keeping friendships.
  • Restricted and repetitive behaviors: stereotyped movements (hand flapping, rocking, spinning), echolalia, lining up objects, insistence on sameness and extreme distress at small changes in routine, highly restricted intense interests, and sensory seeking or avoiding.
  • 🚩 Red flags that require immediate evaluation: no babbling or gesturing by 12 months · no single words by 16 months · no two-word spontaneous phrases by 24 months · ANY loss of language or social skill at any age.
  • 🧪 Screening: M-CHAT-R at the 18-month and 24-month well-child visits (universal screening), then referral for full evaluation (ADOS-2, developmental history). Always test hearing before attributing language delay to autism.
  • Severity is rated by the level of support required (Level 1 requiring support → Level 3 requiring very substantial support), not by an outdated label.
  • 📈 Signs of distress or deterioration in the hospital: increased stereotypies, escalating self-injurious behavior (head banging, biting, hitting), aggression, elopement attempts, and refusal of food or fluids. These are usually communication — pain, overload, or a broken routine — not defiance.
3 · How do you fix it?
  • There is no cure; the goal is function, communication, safety, and reducing distress. Start every encounter by asking the caregiver what the child's routine is, how they communicate, what soothes them, what triggers them, and what words they use for pain and the bathroom.
  • Maintain routine and sameness relentlessly: consistent caregivers and consistent schedule, the same room, the same order of care, one change at a time, and advance warning before transitions. Use a visual schedule and picture cards; many children use PECS or a communication device — bring it with them.
  • Language: short, concrete, literal. Avoid idioms, sarcasm, and figures of speech — "the doctor will be here in a minute" and "this will just be a little stick" are heard literally. Say exactly what will happen, in order, and allow extra processing time after each sentence.
  • Reduce the sensory load: quiet, dim, private room away from the nursing station; cluster care to minimize interruptions; ask before touching; allow noise-canceling headphones, sunglasses, weighted blanket, and the comfort object or favorite toy at all times. Consider a pre-visit tour or social story before a procedure.
  • Safety is a major nursing priority: elopement/wandering (door alarms, ID bracelet, supervision, notify security), self-injurious behavior (padding, helmets, identify and remove the trigger, protect without restraining if at all possible), and unusual pain expression — a child may show pain as agitation or stillness rather than crying, so use observational pain scales and the parent's report.
  • 💊 No medication treats autism itself. Risperidone and aripiprazole are FDA approved for irritability and aggression associated with autism (watch weight, metabolic effects, and EPS). Others target comorbidities: SSRIs for anxiety and repetitive behavior, stimulants or alpha-2 agonists for ADHD symptoms, melatonin for sleep. Applied behavior analysis (ABA), speech-language therapy, occupational therapy for sensory integration, and early intensive intervention are the core treatments — earlier is better, which is why the 18- and 24-month screening matters.
4 · Who is involved?
  • Parents / caregivers — the experts on this child. They are not visitors; get them at the bedside and follow their instructions on routine and communication.
  • Developmental pediatrician / psychiatrist — diagnosis, severity level, comorbidity management, medication for irritability.
  • Speech-language pathologist — expressive and receptive communication, AAC devices, and feeding/swallowing.
  • Occupational therapist — sensory integration, ADLs, fine motor skills, and building the sensory plan the nurse follows.
  • ABA therapist / behavior analyst — skill building and reducing self-injury and aggression through functional behavior assessment.
  • School (IEP team) and early intervention services — legally mandated services from birth to 3 and then through school; also respite care and family support, because caregiver strain is severe and chronic.
5 · How can it get worse / be prevented?
  • 🚨 Wandering and drowning — elopement is common and drowning is a leading cause of death in autistic children. Teach swim lessons, pool fencing, door and window alarms, ID and GPS devices, and notifying neighbors and local police.
  • 🚨 Self-injurious behavior causing real harm, and aggression as the family's crisis point. Both are usually driven by pain, communication failure, or sensory overload — find the function before you medicate.
  • ⚠️ Missed medical illness — a nonverbal child with a UTI, dental abscess, constipation, or ear infection may present only as behavior change. Always rule out pain and physical illness before calling new agitation "autism behavior".
  • ⚠️ Feeding selectivity → nutritional deficiencies; sleep disorders; seizures emerging in adolescence; and anxiety and depression, which are very common and under-recognized in verbal autistic teens and adults.
  • ✅ Teach families: early intensive intervention improves outcomes; keep routines and prepare for changes with social stories; home safety including locks, alarms, and water safety; and be skeptical of "cures" — chelation, bleach protocols, and restrictive unproven diets are ineffective and some are dangerous.
  • ✅ Teach caregivers to advocate: carry a one-page profile of the child's communication, triggers, and comforts to every appointment; request the first or last appointment slot to minimize waiting; and ask for a quiet room. Support the caregivers themselves — burnout, marital strain, and sibling needs are part of this diagnosis.
⭐ If you only remember one thing: Keep the routine, cut the sensory input, use short literal language, and keep the comfort object and the caregiver present. Screen with M-CHAT at 18 and 24 months; any loss of language or social skill at any age is a red flag. New agitation means look for pain or illness first.

🩺 Somatic Symptom Disorder

One-line hook: the symptoms are real and the suffering is real — what is disproportionate is the thought, feeling, and behavior wrapped around them. Nothing here is faked; that is what separates it from factitious disorder and malingering.

1 · What is happening in the body?
  • Emotional distress is expressed through the body. Feelings that cannot be named or tolerated get routed into physical sensation — the pain is generated by real neurologic and autonomic processes, it just is not caused by the disease the patient fears.
  • Amplified interoception — the brain's threat system tags ordinary body signals (a normal heartbeat, gut motility, a muscle twinge) as dangerous, which raises anxiety, which raises sympathetic tone, which makes the sensation stronger. A closed loop.
  • Primary gain = the symptom keeps the unbearable feeling out of awareness. Secondary gain = the attention, care, and escape from obligations the symptom brings. Neither is conscious or deliberate.
  • Common backgrounds: childhood illness or abuse, alexithymia (difficulty identifying and naming emotions), family models of illness behavior, and cultures where physical complaints are more acceptable than emotional ones.
  • The related disorders — know the distinctions:
    • Somatic symptom disorder — one or more distressing physical symptoms plus excessive thoughts/anxiety/time devoted to them, 6 months or more.
    • Illness anxiety disorder — preoccupation with having or getting a serious illness with minimal or no actual symptoms; either care-seeking or care-avoidant.
    • Conversion disorder (functional neurological symptom disorder) — neurologic deficits (paralysis, blindness, nonepileptic seizures, aphonia) that are internally inconsistent and incompatible with known disease; classically follows a stressor; sometimes accompanied by la belle indifférence (surprising lack of concern).
    • Factitious disorder — symptoms are intentionally produced or faked, and the motive is the sick role itself, not an external reward. Factitious disorder imposed on another (formerly Munchausen by proxy) is child abuse and is legally reportable.
    • Malingering — intentional production of symptoms for an external incentive (money, drugs, avoiding work, jail, or military duty). This is not a mental disorder at all.
  • The two questions that sort all of these: is the symptom intentional, and what is the goal? Somatic = unintentional. Factitious = intentional, goal is the sick role. Malingering = intentional, goal is an external reward.
2 · How do you know?
  • Excessive and persistent thoughts about symptom seriousness, persistently high health anxiety, or excessive time and energy devoted to symptoms or health concerns — at least one of those three is required, and it is the criterion that actually defines the disorder.
  • The classic history: a long, thick chart, multiple providers, repeated negative workups, multiple diagnostic tests and procedures, frequent ED visits, and vague or shifting symptoms. Often several unexplained surgeries.
  • Listen for the language: dramatic or vague descriptions, symptoms that do not follow anatomic patterns, and a focus on the symptom rather than on function.
  • Assess what the symptom does for the patient: what happens at home when the pain starts? What does the patient miss or avoid? — this identifies the secondary gain without accusing anyone.
  • 🚨 You still have to rule out disease every time. These patients get real illnesses too, and the biggest clinical danger is the anchoring bias that dismisses a new symptom as "their usual" — assess objectively and document.
  • 📈 Deterioration: escalating opioid or benzodiazepine use, iatrogenic injury from repeated procedures, growing disability and housebound status, and depression and suicide risk, which are elevated.
3 · How do you fix it?
  • Structure the care, do not chase the symptom: one primary provider coordinating everything, and regularly scheduled brief appointments on a fixed schedule rather than PRN visits driven by symptoms. This is the core intervention — it decouples getting care from having symptoms, so the symptom stops being the ticket to attention.
  • Acknowledge the symptom as real, then shift the goal from cure to function. Say: "I believe the pain is real. Let's work on what you can do despite it." The target is functioning, coping, and quality of life — not eliminating the sensation.
  • Limit the time spent discussing symptoms and then redirect deliberately to feelings, stressors, and coping. Ask about what was happening in their life when the symptom started or worsened. Do not reinforce with prolonged attention every time symptoms are described.
  • What NOT to say: Never tell a patient the symptoms are "all in your head," imaginary, or not real, and never confront or accuse them of faking — you will lose them, they will find another provider, and the cycle restarts with a new set of tests. Also avoid false reassurance ("there's nothing wrong with you, you're fine") — it does not reassure and it invalidates.
  • Reduce iatrogenic harm: minimize unnecessary tests, procedures, and specialist referrals; avoid opioids and benzodiazepines; do not order a test just to prove nothing is wrong, because a negative test relieves anxiety only briefly and reinforces the checking cycle.
  • 💊🧠 CBT is the treatment with the best evidence (symptom reappraisal, activity pacing, graded exposure to activity), plus mindfulness and relaxation training. SSRIs and SNRIs help the underlying anxiety and depression and reduce symptom preoccupation; duloxetine also helps chronic pain. Physical therapy is central in conversion disorder — it gives the body a face-saving path back to function.
4 · Who is involved?
  • One designated primary care provider — the gatekeeper who holds the plan and prevents the patient from being fragmented across a dozen specialists.
  • Nurse — the consistent, non-judgmental presence; scheduled check-ins; redirecting to feelings and coping; monitoring for real new disease; and modeling for the rest of the team how to respond without reinforcing.
  • Mental health therapist — CBT, emotion identification, stress management. The referral must be framed as "adding support for the stress of living with these symptoms," not as "you need a psychiatrist because it isn't real."
  • Physical and occupational therapy — graded return to activity, especially in conversion disorder where function returns through the body rather than through insight.
  • Psychiatrist — SSRIs/SNRIs, and managing comorbid depression, anxiety, and personality disorder.
  • Family — teach them to respond warmly to the person and neutrally to the symptom, and to stop taking over the patient's responsibilities, because that is the secondary gain that maintains it. Consistency across the family matters as much as consistency across the team.
5 · How can it get worse / be prevented?
  • 🚨 Iatrogenic injury — the biggest danger. Unnecessary surgeries, adhesions, procedure complications, radiation exposure, and opioid and benzodiazepine dependence created by well-meaning providers who kept trying to fix something.
  • 🚨 Missing real disease in a patient with a somatic diagnosis. Every new or changed symptom gets an objective assessment. Do not let the chart make the diagnosis for you.
  • ⚠️ Progressive disability — deconditioning, job loss, social withdrawal, and a life fully organized around illness. The longer it runs, the harder it is to reverse, so early recognition matters.
  • ⚠️ Depression, anxiety, and suicide risk are elevated — screen directly rather than assuming the distress is only about the symptom.
  • ✅ Teach the patient: stress and emotion produce genuine physical symptoms through real physiologic pathways — this is not the same as being imaginary; keep the scheduled appointments even on good days; keep a symptom-and-stress diary to see the connection; stay physically active and keep a routine; and use the coping skills instead of a new test.
  • ✅ Teach family: attend to the person, not the symptom; do not reward illness behavior with extra attention or by taking over their tasks; encourage independence and activity; and do not argue about whether the symptom is real.
⭐ If you only remember one thing: The symptoms are real and unintentional — never say "it's all in your head." The intervention is one provider, regularly scheduled brief visits (not PRN), acknowledge the symptom, then redirect to feelings, coping, and function. Somatic = unintentional · Factitious = intentional for the sick role · Malingering = intentional for an external reward.

🕯️ Grief vs Depression

One-line hook: grief comes in waves and the self stays intact; depression is a flat unbroken ceiling and the self is worthless. Grief is a normal process that needs presence, not medication.

1 · What is happening in the body?
  • Grief is an attachment response, not a disease. The brain has built a model of the world that contains the person; every reminder collides with their absence, and the yearning is the attachment system searching for someone who does not come back.
  • Acute grief produces real physiologic effects — sleep disruption, appetite loss, fatigue, chest tightness, "air hunger," poor concentration, elevated cortisol, and increased cardiac events (takotsubo/stress cardiomyopathy is real). Treat the body while you support the mind.
  • Grief arrives in waves triggered by reminders, with functional periods in between. That wave pattern is the single most useful physiologic distinction from depression, which is continuous and unbroken.
  • Kübler-Ross stages: denial · anger · bargaining · depression · acceptance. They are not linear, not required, and not a checklist — a patient can skip stages, revisit them, or feel two at once. Originally described for the dying patient, later applied to survivors. Also know Worden's tasks: accept the reality, process the pain, adjust to the new environment, and find an enduring connection while moving forward.
  • Types of grief: anticipatory (begins before the death, common in caregivers and in terminal illness) · disenfranchised (not socially recognized — a pet, a miscarriage, an ex-spouse, an affair partner, a person lost to overdose or suicide) · complicated/prolonged · masked (expressed as physical symptoms or behavior the person does not connect to the loss).
  • Prolonged grief disorder is now a diagnosis: intense yearning and preoccupation with the deceased plus marked impairment persisting at least 12 months in adults (6 months in children and adolescents).
2 · How do you know?
  • ⭐ SIDE BY SIDE — the comparison they test:
    • Mood pattern — Grief: comes in waves/pangs triggered by reminders, with intervals of normal feeling and even laughter. Depression: persistent and unremitting, present most of the day nearly every day.
    • Self-esteem — Grief: preserved; the person still values themselves. Depression: worthlessness and self-loathing — this is one of the sharpest dividing lines.
    • Guilt — Grief: specific and about the loss ("I should have taken her to the doctor sooner"). Depression: global and pervasive ("I ruin everything, everyone is better off without me").
    • Anhedonia — Grief: pleasure and connection are still possible between waves. Depression: pleasure is gone across the board.
    • Thoughts of death — Grief: focused on joining or being with the deceased, or wishing they had died instead; usually without plan or intent. Depression: a wish to be dead because of worthlessness, and active suicidal ideation with a plan.
    • Course — Grief: intensity decreases over weeks to months; functioning gradually returns. Depression: stays the same or worsens without treatment.
    • Response to support — Grief: comforted by presence and connection. Depression: support does not reach them; often withdraws from it.
    • Perceptions — Grief: briefly hearing or seeing the deceased is normal and culturally common. Depression: mood-congruent psychosis is a severe symptom.
  • ⚠️ They can coexist. A bereaved person can develop major depression, and prior depression makes it likelier. Do not withhold treatment because a loss "explains" it — assess for the depression criteria on their own merit.
  • 🚩 Warning signs of prolonged or complicated grief: the room untouched for a year, inability to say the person died, complete avoidance of any reminder, persistent inability to work or care for self, and intense unrelenting yearning past a year.
  • 🚨 Always screen for suicide in a bereaved person, especially after the loss of a spouse or a child, after a suicide loss, and in older men living alone. Bereavement raises suicide risk, particularly in the first months.
  • Also assess: substance use starting or increasing, missed medical care, weight loss, and social isolation.
3 · How do you fix it?
  • Normal grief does not need to be fixed — it needs presence. Sit with them, use silence, and let them tell the story as many times as they need to. Repeated retelling is how the loss becomes real; do not redirect them off it.
  • 💬 THERAPEUTIC responses — use these:
    • Silence — allows them to gather thoughts; the hardest and most underused skill.
    • Offering self — "I'll sit here with you." Broad openings — "Tell me what happened." General leads — "Go on."
    • Reflecting / restating — "You feel like you should have known." Exploring — "Tell me more about that." Clarifying — "I'm not sure I follow — do you mean...?"
    • Making observations — "I notice you haven't been eating." Verbalizing the implied — "Are you saying it feels unbearable?"
    • Acknowledging feelings — "That sounds incredibly painful." Focusing — "You mentioned your daughter; let's talk about that."
    • Presenting reality and summarizing at the end so they know they were heard.
  • 💬 NON-THERAPEUTIC responses — these sound caring and are wrong answers:
    • False reassurance — "Everything will be fine," "Don't worry," "You'll feel better soon." It shuts the conversation down and tells them their fear is unwelcome.
    • "Why" questions — "Why do you feel that way?" Demands a justification the patient does not have and puts them on the defensive. Ask "what" or "tell me about" instead.
    • Giving advice — "If I were you, I'd..." Takes the decision away and makes them dependent on you. Explore their options instead.
    • Minimizing / clichés — "At least she isn't suffering," "He's in a better place," "You still have your other children," "I know exactly how you feel." All of these dismiss the loss.
    • Approval or disapproval — "That's good," "You shouldn't feel that way." Changing the subject. Defending the staff, the doctor, or God. Challenging or arguing. Probing for details out of curiosity. Belittling ("everyone gets sad sometimes"). Stereotyped or automatic replies ("keep your chin up," "it's God's plan").
    • Requesting an explanation, giving literal responses to figurative statements, and testing or challenging the patient's perception.
  • Practical grief care: normalize the symptoms ("waves, poor sleep, and forgetting things are all expected"); support sleep, food, and fluids; help with the concrete tasks that are overwhelming; encourage rituals and memory-making; discourage major irreversible decisions in the first year (selling the house, moving, remarrying); and respect cultural and religious mourning practices without assuming what they are — ask.
  • 💊 Do not medicate normal grief. Antidepressants do not treat grief and there is no evidence they help uncomplicated bereavement. Never routinely prescribe benzodiazepines for acute grief — they blunt the emotional processing that grief requires and carry dependence risk. Do treat major depression, prolonged grief disorder, and PTSD when they are present — with SSRIs plus therapy, and use complicated grief treatment or grief-focused CBT for prolonged grief.
4 · Who is involved?
  • Nurse — often the person present at the death and in the hours after; provides presence, honest information, and the first assessment of how this family is coping. What you say in that first hour is remembered for decades.
  • Chaplain / spiritual care — rituals, meaning-making, and religious practices around death, regardless of the family's affiliation.
  • Social worker — funeral arrangements, benefits, guardianship, and the practical avalanche that follows a death.
  • Hospice and palliative care and their bereavement programs — hospice provides bereavement follow-up for the family for about 13 months after the death, which is a commonly tested detail.
  • Therapist / grief counselor — for prolonged grief, traumatic loss, and coexisting depression or PTSD.
  • Support groups and peer support — bereaved parents, widow/widower groups, suicide-loss survivor groups. Child life specialists for grieving children, and school counselors. Include the children — they grieve too and need age-appropriate, concrete, honest language.
5 · How can it get worse / be prevented?
  • 🚨 Suicide — the risk rises after bereavement, especially after the death of a spouse or a child, after a suicide loss, and in older men. Ask directly.
  • 🚨 Prolonged grief disorder — beyond 12 months in adults, with intense yearning, identity disruption, avoidance, and functional impairment. Risk factors: sudden or violent death, death of a child, dependent relationship, poor support, and prior mental illness.
  • ⚠️ Physical consequences: increased cardiac events in the first months ("broken heart" cardiomyopathy), immune suppression, neglected chronic conditions and missed medications, weight loss, and higher mortality in the surviving spouse in the first year.
  • ⚠️ Substance use starting or escalating, and disenfranchised grief going unsupported because no one recognized the loss as legitimate — miscarriage, pet death, overdose loss, or the loss of a partner in a relationship the family did not accept.
  • ✅ Teach the bereaved: there is no timetable and no right way to grieve; waves are normal and so is laughing; anniversaries, birthdays, and holidays will hurt and can be planned for; eat, sleep, and keep taking your own medications; delay big decisions; and it is normal to briefly hear or see the person.
  • ✅ Teach when to seek help: persistent hopelessness, worthlessness, no improvement at all after several months, inability to function, increasing alcohol use, or any thought of suicide — and give them 988. Teach family and friends what to actually say: show up, say the person's name, and offer a specific concrete task rather than "let me know if you need anything."
⭐ If you only remember one thing: Grief = waves, intact self-esteem, comforted by others, improves over time. Depression = constant, worthless, unreachable, does not improve. Presence and silence are the intervention — false reassurance, "why" questions, giving advice, and clichés are never therapeutic — and normal grief is not treated with medication.
Study material only — always check your course materials and facility policy.