A Working Clinical Psychiatry Reference
A desk reference for a practising clinician, framed for European (Romanian) practice — ICD-10 diagnosis, psychopharmacology, and prescribing safety. This is a living scaffold: the structure and a safe orientation layer are here; the book-deep detail goes into the labelled slots you fill from your own Maudsley, Stahl, and DSM-5-TR. It runs from Part 0 (Orientation) through a diagnostic browser (I), the pharmacology foundations and drug classes (II–III), safety & emergencies (IV), assessment (V), treatment algorithms (VI), special populations & monitoring (VII), and a brief therapies orientation. Part I is a searchable, two-tier disorder browser — every ICD-10 F-block is a collapsible section of cards, anchored to its F-code and paraphrased from the Blue Book. Three sourced deep-dive dossiers — binding affinities (Ki), side-effect/CYP detail, and a receptor-mechanism synthesis — fold into the foundations they belong to in Part II. Navigation is built in: a chapter launchpad at the top jumps to any part, and the page search finds any disorder, drug, F-code, or red flag and lists matches to pick from. Empty slots throughout hold your book-deep detail; print expands everything and drops the navigation.
Drafted by Claude (Opus 4.8, Anthropic) on 8 June 2026, for a practising clinician's personal use. An orientation aid, not a clinical authority — verify all doses, criteria, and interactions against current primary sources before any clinical decision.
0Orientation
How to use this page. A cheatsheet for the desk, not a textbook. Two ways in: the chapter launchpad at the top jumps to any part, and the search box finds a disorder, drug, F-code, or red flag anywhere on the page and lists the matches — pick one to jump to it. Open the page to re-anchor a code, a criteria scaffold, a receptor profile, a monitoring interval, or a red flag — then go to the primary source. Diagnostic criteria are paraphrased, never reproduced; every load-bearing number is cited to a current source or deferred to where you'll confirm it. The page is designed to grow: see "How to expand" below.
How to use & the safety contract
This is an orientation aid for a clinician, not a substitute for current guidelines, the SmPC / product label, your local (Romanian / EU) formulary, or clinical judgement. Every dose, plasma level, titration step, monitoring interval, threshold, washout, and interaction must be confirmed against a primary source before any clinical decision. Specific drug doses are intentionally not asserted by the author of the scaffold — they live in slots you fill from the SmPC (EMA → ANMDMR) or the Maudsley Guidelines. Where guidance differs by jurisdiction (Romania/EU · UK NICE · Canadian CANMAT · US APA), that is flagged rather than presented as universal. Nothing here is patient-facing.
What’s on this page
Beyond the reading text, the page is a small set of working tools. Here is everything you can actually do with it — each links straight to the feature.
| Tool | What it does | Where |
|---|---|---|
| Page search | Type a disorder, drug, F-code, red flag, or interaction and get a live autocomplete list of matches anywhere on the page — pick one to jump to it. | search box (top) |
| Chapter launchpad | A landing grid that jumps to any of the nine parts in one click; collapses out of the way once you’re reading. | top of the page |
| Disorder browser | A searchable, two-tier browser of every ICD-10 F-block — collapsible sections of cards, each anchored to its F-code, paraphrased from the Blue Book, with a DSM-5-TR pointer and the ICD-vs-DSM divergence. Filter by category or expand a card. | Part I |
| Binding-affinity (Ki) dossier | A sourced master table of receptor/transporter affinities across all drug classes, with verified-vs-attributed tagging — folds open as a deep-dive annex. | Part II · Ki dossier |
| Side-effects & CYP dossier | Within-class differences in half-life, side-effect profile and cytochrome-P450 interactions, in depth. | Part II · side-effect dossier |
| Receptor-mechanism synthesis | A treatment-back-to-hypothesis synthesis of receptor mechanisms across disorders. | Part II · mechanism dossier |
| Rating-scale pointer & score calculators | A copyright-aware catalogue of common instruments (what each measures, how to obtain it, licensing) — plus interactive scorers for the free scales (PHQ-9, GAD-7, AUDIT, YMRS, CIWA-Ar, BPRS) that total and band live as you enter items. | Part V · scales & calculators |
| Safety & emergency reference | High-yield red-flag syndromes (serotonin syndrome, NMS, lithium toxicity, withdrawal states and more) for rapid re-anchoring at the desk. | Part IV |
| Treatment algorithms | Condition-by-condition treatment-pathway scaffolds you can step through. | Part VI |
| Theme & print | Light / dark / auto theme toggle (remembered between visits); printing expands every collapsible block and drops the navigation for a clean paper copy. | top of the page |
How to expand this page
Empty, dashed boxes marked with a source tag are expansion slots — paste your own detail there from the books you own. The orientation prose around them is the safe scaffold; the depth is yours. Source tags tell you what belongs where: MAUDSLEY (dosing, titration, prescribing tables) · STAHL (mechanism, receptor diagrams in prose) · DSM-5-TR WORDING (exact criteria phrasing) · SmPC / ANMDMR (Romanian label specifics) · YOUR NOTES (clinical pearls, local pathways).
(1) When you fill a slot, change its class from slot to slot filled — the border turns solid and it reads as finished content; empty ones stay visibly "to do". (2) Every slot has a comment marker above it; search @@EXPAND in any editor to jump between all the gaps. (3) Copy the depression block (disorder template) or the lithium block (drug template) as your pattern for new entries. The minimal slot looks like:
It stays one self-contained file: edit, save, re-host (Neocities / Cloudflare / GitHub Pages) exactly as the other volumes. Content you paste from your books is your private working copy — don't redistribute it.
ICD-10, DSM-5-TR, and ICD-11
↗ ICD-10 browser (Chapter V, F-codes) · ↗ ICD-10 "Blue Book" (CDDG, free WHO PDF) · ↗ DSM-5-TR (APA)
ICD-10 leads here — it is what Romania codes and reports. Each disorder is anchored to its F-code (deep-linked into the WHO browser) with criteria paraphrased from the free, official ICD-10 Blue Book (Clinical Descriptions and Diagnostic Guidelines). DSM-5-TR is the wording cross-reference (research literature, most operationalised phrasing — cite the section, never reproduce). ICD-11 (in force at WHO since 2022) is noted where it changes things, as the coming successor while the EU transitions. Divergences (e.g. schizophrenia duration, depression symptom structure) are flagged disorder-by-disorder — that contrast is clinically useful.
European / Romanian framing
The regulatory source for a dose in Romania is the SmPC / RCP (Rezumatul Caracteristicilor Produsului). For centrally authorised drugs the SmPC is on the EMA EPAR page (all EU languages); for nationally authorised products use the EMA national-registers gateway to reach ANMDMR (anm.ro).
↗ EMA — national medicine registers · ↗ ANMDMR (Romania) · ↗ EMA medicines (EPAR / SmPC)
The Maudsley Guidelines are the de-facto prescribing reference but are UK; NICE and BAP are UK; CANMAT is Canadian; APA is US. All are excellent and widely used across Europe, but none is Romania's regulatory authority — reconcile any dose/indication with the Romanian SmPC. There is no single EU-wide psychiatric prescribing guideline. Controlled-drug scheduling and availability (e.g. methylphenidate, lisdexamfetamine, modafinil, some benzodiazepines) differ in Romania — check national availability/scheduling before prescribing.
Abbreviation decoder
| Abbrev. | Meaning |
|---|---|
| SSRI / SNRI | selective serotonin / serotonin–noradrenaline reuptake inhibitor |
| TCA / MAOI | tricyclic antidepressant / monoamine-oxidase inhibitor |
| FGA / SGA | first- / second-generation (typical / atypical) antipsychotic |
| EPS / TD | extrapyramidal side effects / tardive dyskinesia |
| NMS | neuroleptic malignant syndrome |
| QTc | heart-rate-corrected QT interval |
| CYP / t½ | cytochrome P450 enzyme / elimination half-life |
| ANC / FBC | absolute neutrophil count / full blood count |
| SmPC / RCP | Summary of Product Characteristics (EN) / Rezumatul Caracteristicilor Produsului (RO) |
| CDDG | Clinical Descriptions & Diagnostic Guidelines (the ICD-10 "Blue Book") |
| prn | pro re nata — as required |
| TRD / TRS | treatment-resistant depression / schizophrenia |
IDiagnostic framework
A searchable browser of the ICD-10 diagnostic groups. Each card is anchored to its F-code (deep-linked into the WHO browser) with criteria paraphrased from the free Blue Book (CDDG), a DSM-5-TR pointer, and the ICD-10-vs-DSM divergence — never the verbatim criterion sets. Search by name, F-code, or keyword, or filter by category; click a card to expand. Cross-check against PsychDB or StatPearls. (No JavaScript? Every card below is still present and expandable directly.)
These cards hold orientation scaffolds in paraphrase, not reproduced DSM-5-TR or ICD-10 criterion text (those are copyrighted/licensed). Use a card to re-anchor a code, a scaffold, a differential, or a red flag — then confirm exact wording in the primary source. Fill each card’s your-notes slot from your own books.
Mood disorders F30–F39 · affective▾
Disorders whose primary disturbance is mood — depressed, elevated, or alternating — with secondary changes in activity, cognition, and biology. Residual codes F38 (other mood disorders, incl. recurrent brief depressive and mixed affective episode) / F39 (unspecified) carry the leftovers.
↗ WHO block F30–F39 · DSM-5-TR: split into Depressive Disorders and Bipolar & Related Disorders (two separate chapters)
Manic episodeF30▾
↗ F30 (.0 hypomania · .1 mania without psychosis · .2 mania with psychosis)
ICD-10 view
A distinct period of elevated/irritable mood with increased energy/activity, plus inflated self-esteem, reduced sleep need, pressured speech, racing thoughts, distractibility, risk-taking. Mania: marked impairment / psychosis / hospitalisation. Hypomania (F30.0): lesser, no marked impairment or psychosis. A single manic episode is coded here; recurrence with any prior mood episode moves to bipolar (F31).
DSM-5-TR view — paraphrase (orientation; verbatim criteria belong in your licensed source)
A. Abnormally elevated/expansive or irritable mood with persistently increased activity/energy, ≥ 1 week (or any duration if hospitalised).
B. ≥ 3 of the following (≥ 4 if mood is only irritable):
- inflated self-esteem / grandiosity
- decreased need for sleep
- more talkative / pressured speech
- flight of ideas / racing thoughts
- distractibility
- increased goal-directed activity or psychomotor agitation
- excessive involvement in high-risk activities
C. Marked impairment, hospitalisation, or psychosis. Hypomania = ≥ 4 days, no marked impairment, no psychosis.
▸ Differs from ICD-10: DSM centres the activity/energy criterion (added in DSM-5 — mood change alone is insufficient); ICD-10 treats raised energy as one feature among several. A standalone manic episode in DSM is classed as bipolar I rather than its own category.
Paste your licensed DSM-5-TR criterion wording and specifiers here; the view above is orientation only.
Psychotic mania, severe risk-taking, exhaustion/dehydration, aggression. Exclude substance-induced (stimulants, steroids) and organic mania (frontal lesion, hyperthyroidism).
Bipolar affective disorderF31▾
↗ F31 (typed by current episode: hypomanic, manic, depressive, mixed, remission)
ICD-10 view
Two or more episodes in which mood and activity are significantly disturbed — at least one of which is (hypo)manic, with depressive episodes at other times. Coded by the current episode type and severity. ICD-10 has no separate "bipolar II" category: hypomania-plus-depression is captured here under F31, not as a distinct diagnosis.
DSM-5-TR view — paraphrase
Bipolar I = ≥ 1 lifetime manic episode (depression not required for the diagnosis). Bipolar II = ≥ 1 hypomanic episode and ≥ 1 major depressive episode, never a full manic episode — a distinct category, not "milder bipolar I." Specifiers: with anxious distress, mixed features, rapid cycling, melancholic, psychotic, peripartum, seasonal.
▸ Differs from ICD-10: the big one — DSM has a clean bipolar II as its own diagnosis; ICD-10 folds hypomania+depression into F31 without naming bipolar II. DSM also requires the activity/energy criterion for the index manic/hypomanic episode.
Paste your licensed wording here.
Screen any depression for past (hypo)mania before an antidepressant — missed bipolarity risks switch/cycling. Red flags: mixed features (high suicide risk), rapid cycling, psychotic episodes, postpartum onset.
Depressive episodeF32▾
↗ F32 (.0 mild · .1 moderate · .2 severe without psychosis · .3 severe with psychosis)
ICD-10 view
ICD-10 builds it from three typical symptoms — depressed mood, loss of interest/enjoyment, reduced energy/fatigue — plus common additional symptoms (reduced concentration, low self-worth/guilt, bleak/pessimistic views, self-harm ideas, disturbed sleep, reduced appetite). Duration ≥ 2 weeks. Severity by count: mild (≈ 2 typical + 2 others), moderate (≈ 2 typical + 3–4), severe (3 typical + ≥ 4), severe further split by psychotic features. Function impaired; not better explained by substances/organic cause.
DSM-5-TR view — paraphrase (orientation; verbatim criteria belong in your licensed source)
A. ≥ 5 of the following in the same 2-week period, a change from baseline; ≥ 1 must be (1) or (2):
- depressed mood (cardinal)
- markedly diminished interest/pleasure — anhedonia (cardinal)
- significant appetite or weight change
- insomnia or hypersomnia
- psychomotor agitation or retardation (observable)
- fatigue / loss of energy
- worthlessness or excessive/inappropriate guilt
- reduced concentration or indecisiveness
- recurrent thoughts of death / suicidal ideation
B. Significant distress or functional impairment. C. Not attributable to a substance or another medical condition. (D/E: not better explained by a schizophrenia-spectrum disorder; never a manic or hypomanic episode.)
Specifiers: severity; with anxious distress, mixed, melancholic, atypical, psychotic, peripartum features; seasonal pattern.
▸ Differs from ICD-10: ICD-10 builds depression from 2-of-3 typical symptoms + others, graded by count, vs DSM's ≥ 5 of 9 with a cardinal.
DSM-5 removed the bereavement exclusion (DSM-IV barred an MDE diagnosis within ~2 months of a loss): a major depressive episode can now be diagnosed during grief, with a footnote to help distinguish normal grief from MDE. ICD-10's guidance treats uncomplicated bereavement as a normal reaction (codeable under Z63.4 rather than a depressive episode). (Note: prolonged grief disorder is a separate DSM-5-TR addition — see Stress & trauma.)
Premenstrual dysphoric disorder is a DSM-5 depressive disorder (mood/irritability/anxiety symptoms tied to the luteal phase, remitting after menses). WHO ICD-10 has no PMDD code in the F-chapter; it sits in the gynaecological chapter as premenstrual tension syndrome (N94.3). (ICD-11 adds PMDD.)
Paste your licensed wording and specifier set here.
Bipolar depression (screen for past hypomania), dysthymia (F34.1), adjustment disorder, organic/secondary mood disorder (thyroid, steroids, anaemia, B12), substance-related. Red flags: suicidality, psychotic features, catatonia, severe self-neglect, postpartum onset.
Add exact ICD-10 Blue Book symptom-counts, your PHQ-9 / HADS cut-offs, local pathway pointer.
Recurrent depressive disorderF33▾
↗ F33 (typed by current episode severity / remission)
ICD-10 view
Repeated depressive episodes (as in F32) without any history of independent (hypo)mania. Coded by the severity of the current episode and remission status. The recurrence itself, plus the absence of mania, is what distinguishes it from a single F32 episode and from bipolar disorder.
DSM-5-TR view — paraphrase
DSM doesn't separate single vs recurrent into different codes the way ICD does — it's one diagnosis (major depressive disorder) specified as single episode or recurrent episodes (≥ 2, separated by ≥ 2 months without criteria met), plus severity / remission / feature specifiers.
▸ Differs from ICD-10: ICD-10 gives single (F32) and recurrent (F33) separate code families; DSM treats recurrence as a specifier on one MDD diagnosis. Clinically equivalent, structurally different.
Paste your licensed wording here.
Recurrence drives maintenance-treatment decisions; document episode count and inter-episode recovery. Always re-screen for emergent bipolarity at each new episode.
Persistent mood disordersF34▾
↗ F34 (.0 cyclothymia · .1 dysthymia)
ICD-10 view
Cyclothymia (F34.0): persistent instability of mood — numerous periods of mild depression and mild elation, none severe or long enough to meet bipolar/recurrent-depressive criteria. Dysthymia (F34.1): chronic (≥ 2 years) low-grade depressed mood not meeting the threshold for a depressive episode. Both are long-standing, fluctuating, sub-threshold conditions.
DSM-5-TR view — paraphrase
Persistent depressive disorder (dysthymia): depressed mood most days for ≥ 2 years (≥ 1 year in youth) plus ≥ 2 of (appetite, sleep, energy, self-esteem, concentration, hopelessness); DSM-5 merged chronic MDD and dysthymia into this single label. Cyclothymic disorder: ≥ 2 years of numerous hypomanic and depressive periods, neither meeting full episode criteria.
▸ Differs from ICD-10: DSM consolidated chronic MDD + dysthymia into "persistent depressive disorder," a merge ICD-10 didn't make (it keeps dysthymia distinct from recurrent depression).
Disruptive mood dysregulation disorder (chronic severe irritability + frequent temper outbursts, onset before age 10) is a DSM-5 depressive disorder, created to curb over-diagnosis of paediatric bipolar. WHO ICD-10 has no DMDD code. (US ICD-10-CM places it at F34.81; ICD-11 covers similar presentations under oppositional defiant disorder with chronic irritability-anger.)
Paste your licensed wording here.
Anxiety & phobic disorders F40–F41 · neurotic▾
Excessive, persistent fear or anxiety and avoidance, out of proportion to actual threat, causing distress or impairment — distinguished by the focus of the fear. F40–F48 is ICD-10's "neurotic, stress-related & somatoform" block; the OCD, stress, and somatoform sections that follow are its neighbours.
↗ WHO block F40–F48 · DSM-5-TR: Anxiety Disorders (its own chapter)
Phobic anxiety disordersF40▾
↗ F40 (.0 agoraphobia · .1 social phobia · .2 specific/isolated phobia)
ICD-10 view
Anxiety triggered by well-defined situations or objects that are not inherently dangerous, leading to avoidance or dread. Typed by focus: agoraphobia (F40.0) — fear of open spaces, crowds, public places, situations where escape is hard (ICD-10 codes it with or without panic); social phobia (F40.1) — fear of scrutiny by others; specific phobia (F40.2) — a circumscribed object or situation.
DSM-5-TR view — paraphrase (orientation; verbatim criteria belong in your licensed source)
Marked, persistent (typically ≥ 6 months) fear of a specific situation/object, near-always provoked, actively avoided or endured with intense distress, out of proportion, causing impairment. Agoraphobia: fear of ≥ 2 of — public transport, open spaces, enclosed spaces, queues/crowds, being outside the home alone. Social anxiety disorder: fear of social/performance scrutiny. Specific phobia: animal, natural-environment, blood-injection-injury, situational, other.
▸ Differs from ICD-10: DSM-5 unbundles agoraphobia from panic disorder — they are two independent diagnoses that can be coded together; ICD-10 nests panic within agoraphobia (F40.0 "with/without panic"). DSM also sets an explicit ≥ 6-month duration for all ages.
Paste your licensed wording and the specific-phobia subtypes here.
Panic disorder (F41.0), GAD, PTSD-related avoidance, autistic social difficulty vs social phobia, and physical mimics (see F41 card). First-line treatment is exposure-based CBT.
Other anxiety disordersF41▾
↗ F41 (.0 panic · .1 GAD · .2 mixed anxiety-depressive)
ICD-10 view
Anxiety that is not restricted to a particular situation — free-floating. Panic disorder (F41.0): recurrent unexpected panic attacks (episodic paroxysmal anxiety) with anticipatory fear, not secondary to a phobic situation. GAD (F41.1): persistent, generalised, excessive worry and tension across everyday events, with autonomic and motor symptoms. Mixed anxiety-depressive (F41.2): both anxiety and depressive symptoms present, neither severe enough to justify a separate diagnosis.
DSM-5-TR view — paraphrase
Panic disorder: recurrent unexpected panic attacks + ≥ 1 month of worry about further attacks or maladaptive change in behaviour. GAD: excessive anxiety/worry more days than not for ≥ 6 months, hard to control, with ≥ 3 of — restlessness, fatigue, poor concentration, irritability, muscle tension, sleep disturbance (≥ 1 in children).
▸ Differs from ICD-10: ICD-only: mixed anxiety-depressive disorder (F41.2) has no DSM-5 counterpart — DSM would code the anxiety and depression separately or use "other specified." DSM also treats a panic attack as a cross-cutting specifier that can be attached to any disorder, not only panic disorder.
ICD-10 files separation anxiety (F93.0) and selective mutism (F94.0) under childhood-onset disorders. DSM-5 relocated both into the Anxiety Disorders chapter, recognising separation anxiety can persist or begin in adulthood. (ICD-11 follows DSM.) See the childhood-onset section for the ICD-10 F9x codes.
Paste your licensed panic/GAD wording here.
Exclude hyperthyroidism, arrhythmia, phaeochromocytoma, caffeine/stimulant or substance withdrawal, and depression with anxious distress. Red flags: first panic at older age, exertional symptoms, focal neurology → investigate medically.
Add the DSM panic/GAD criteria wording and your assessment pearls (GAD-7, interoceptive exposure).
Obsessive–compulsive disorder F42 · neurotic▾
Recurrent obsessions and/or compulsions that are time-consuming or impairing. A single 3-character category in ICD-10; the DSM-5 spin-off "related disorders" live as where-it-lives notes below.
↗ WHO F42 · DSM-5-TR: Obsessive-Compulsive & Related Disorders (its own chapter)
Obsessive–compulsive disorderF42▾
↗ F42 (.0 obsessional thoughts · .1 compulsive acts · .2 mixed · .8 other · .9 unspecified)
ICD-10 view
Obsessions (intrusive, distressing thoughts/images/urges recognised as one's own and resisted) and/or compulsions (repetitive acts performed to reduce anxiety, not pleasurable), present on most days for ≥ 2 weeks, time-consuming or impairing, experienced as excessive/unreasonable. Typed by predominant feature: F42.0 predominantly obsessional thoughts/ruminations; F42.1 predominantly compulsive acts/rituals; F42.2 mixed; F42.8 other; F42.9 unspecified.
DSM-5-TR view — paraphrase (orientation; verbatim criteria belong in your licensed source)
A. Obsessions, compulsions, or both. B. Time-consuming (a useful rule-of-thumb is > 1 hour/day) or causing significant distress/impairment. C. Not attributable to a substance or medical condition. D. Not better explained by another disorder. Specifiers: insight — good/fair, poor, or absent/delusional; and tic-related (current or past tic disorder).
▸ Differs from ICD-10: DSM requires obsessions or compulsions or both (ICD-10's F42.0/.1/.2 typing by predominance is gone — DSM uses a single category with specifiers). DSM has no minimum-duration rule (ICD-10 uses ≥ 2 weeks) but emphasises the > 1-hour/day burden, and adds the insight and tic-related specifiers ICD-10 lacks.
DSM-5's OCRD chapter also contains body dysmorphic disorder, hoarding disorder, excoriation (skin-picking) disorder, and trichotillomania (hair-pulling). In WHO ICD-10: BDD sits under hypochondriacal disorder (F45.2); trichotillomania is a habit/impulse disorder (F63.3); hoarding and excoriation have no dedicated WHO ICD-10 code (US ICD-10-CM added F42.3 and F42.4, but those are not WHO codes). (ICD-11 brings most of these together in its own OCRD grouping.)
Paste your licensed OCD criteria and the OCRD-chapter definitions (BDD muscle-dysmorphia specifier, hoarding, excoriation, trichotillomania) here.
Distinguish primary OCD from obsessive–compulsive (anankastic) personality disorder (F60.5 — ego-syntonic, no true obsessions/compulsions), from GAD's worry, from depressive ruminations, and from the stereotypies of autism or tic disorders. Absent-insight/delusional OCD is not schizophrenia. First-line: ERP-based CBT; pharmacologically, OCD often needs higher-dose, longer-trial SSRIs (or clomipramine).
Add your high-dose/long-trial SSRI and clomipramine pearls, Y-BOCS use, and OCRD-relative specifics.
Reaction to severe stress & adjustment F43 · neurotic▾
Disorders where an identifiable stressor or trauma is the necessary cause — the condition would not have arisen without it. Residual codes F43.8/F43.9 folded here.
↗ WHO F43 · DSM-5-TR: Trauma- & Stressor-Related Disorders (its own chapter)
Acute stress reactionF43.0▾
A transient reaction to exceptional physical/mental stress in someone without another mental disorder: an initial "daze" with narrowed attention and disorientation, then either withdrawal or agitation. Onset within minutes; symptoms typically begin to settle within hours to a few days. Conceived as a near-normal response, not a sustained disorder.
DSM-5 makes acute stress disorder a standalone diagnosis in the Trauma- & Stressor-Related chapter: exposure to actual/threatened death, serious injury or sexual violence, then ≥ 9 symptoms across five categories (intrusion, negative mood, dissociation, avoidance, arousal) lasting 3 days to 1 month. So the same clinical window is a transient near-normal reaction in ICD-10 but an operationalised diagnosis in DSM-5; DSM no longer treats it as a predictor of PTSD. (ICD-11 moves acute stress reaction out of its disorders grouping entirely.)
Paste your licensed acute stress disorder criteria here.
Post-traumatic stress disorderF43.1▾
ICD-10 view
Arises (usually within ~6 months) of an exceptionally threatening or catastrophic event: persistent re-experiencing (intrusive memories, flashbacks, nightmares), avoidance of reminders, and a state of autonomic hyperarousal (hypervigilance, exaggerated startle, sleep and concentration disturbance), with distress/impairment. Loosely operationalised compared with DSM.
DSM-5-TR view — paraphrase (orientation; verbatim criteria belong in your licensed source)
Exposure to actual/threatened death, serious injury or sexual violence (direct, witnessed, learned-of, or repeated occupational exposure), then symptoms across four clusters: B. intrusion; C. avoidance; D. negative alterations in cognitions and mood; E. alterations in arousal and reactivity. Duration > 1 month; specifiers for dissociative and delayed expression, plus a separate preschool subtype for children ≤ 6.
▸ Differs from ICD-10: DSM adds a whole fourth cluster — negative cognitions/mood — that ICD-10 lacks, and is far more explicit (four clusters, ~20 symptoms). ICD-11 went the opposite way, narrowing PTSD to two symptoms in each of three core clusters and adding a separate complex PTSD for additional self-organisation disturbances — a category DSM-5 declined.
Not in ICD-10 or DSM-5. ICD-11 adds complex PTSD (core PTSD plus affect-regulation, negative self-concept and relational disturbances) as the modern successor to ICD-10's F62.0 enduring personality change after catastrophic experience. DSM-5 chose to absorb such presentations into its broadened PTSD rather than create a separate diagnosis.
Paste your licensed PTSD criteria and the dissociative/delayed/preschool specifiers here.
Adjustment disorder (sub-threshold, no trauma criterion), acute stress reaction/disorder (early window), depression, panic, and dissociative disorders. Screen for comorbid substance use and suicidality. First-line: trauma-focused CBT or EMDR.
Add the DSM cluster wording, complex-PTSD concept, and your assessment pearls.
Adjustment disordersF43.2▾
↗ F43.2 (subtyped by predominant reaction — depressive, anxious, mixed, conduct…)
ICD-10 view
States of subjective distress and emotional disturbance arising while adapting to a significant life change or stressful event, impairing social functioning, with onset usually within 1 month of the stressor and duration usually not exceeding 6 months (longer for a depressive reaction). Subtyped by the predominant reaction (brief/prolonged depressive, mixed anxiety-depressive, with disturbance of conduct, etc.). A diagnosis of exclusion — must not meet the threshold for another disorder.
DSM-5-TR view — paraphrase
Emotional/behavioural symptoms within 3 months of an identifiable stressor, out of proportion or causing significant impairment, resolving within 6 months after the stressor (or its consequences) ends. Subtypes: with depressed mood, with anxiety, mixed, with disturbance of conduct, or unspecified.
▸ Differs from ICD-10: mostly aligned; DSM uses a 3-month onset window vs ICD-10's ~1 month. Both treat it as sub-threshold/residual.
An intense, disabling, persistent grief reaction. Added in ICD-11 and DSM-5-TR (not in ICD-10, where persistent grief would be coded as adjustment disorder or "other reactions to severe stress" F43.8). DSM-5-TR requires ≥ 12 months since the death (≥ 6 months in ICD-11).
Paste your licensed adjustment-disorder and prolonged-grief criteria here.
Normal, proportionate stress responses (not a disorder); major depression or an anxiety disorder when full threshold is met; PTSD when the stressor is traumatic and re-experiencing dominates; uncomplicated bereavement.
Dissociative & somatoform disorders F44–F45 · neurotic▾
Symptoms without an adequate physical explanation — either a loss of psychological integration (dissociative/conversion) or persistent bodily complaints and health anxiety (somatoform).
↗ WHO F44 · ↗ WHO F45 · DSM-5-TR: Dissociative Disorders; Somatic Symptom & Related Disorders (two separate chapters)
Dissociative [conversion] disordersF44▾
Partial or complete loss of the normal integration of memory, identity, sensation, or control of movement, with no physical cause found and a convincing temporal link to stressful events/problems. Includes the conversion presentations (F44.4–.7: psychogenic motor loss, non-epileptic "convulsions", sensory loss) — ICD-10 deliberately keeps conversion here, under dissociation, on the view that they share a mechanism.
DSM-5 keeps dissociative amnesia (with a fugue specifier), dissociative identity disorder (ICD-10's "multiple personality", F44.81 in US ICD-10-CM / under F44.8 in WHO), and depersonalisation/derealisation disorder in a standalone Dissociative Disorders chapter — but moves conversion out, renaming it Functional Neurological Symptom Disorder and placing it among the somatic-symptom disorders, with criteria emphasising positive incompatibility findings on neurological exam rather than a presumed psychological cause.
Always exclude genuine neurological/medical disease first (conversion is not a diagnosis of exclusion alone — it needs positive incompatibility signs). Consider epilepsy vs non-epileptic attacks, malingering and factitious disorder (intentional production — different intent), and organic amnesia.
Paste your licensed dissociative-disorders and functional-neurological-symptom-disorder criteria here.
Somatoform disordersF45▾
Repeated presentation of physical symptoms with persistent requests for investigation, despite repeated negative findings and reassurance. Somatization (F45.0): multiple, recurrent, changing symptoms over ≥ 2 years. Hypochondriacal (F45.2): persistent preoccupation with having a serious illness (includes dysmorphophobia). Autonomic dysfunction (F45.3) and persistent somatoform pain (F45.4) complete the block.
DSM-5 collapsed most of F45: somatization, undifferentiated somatoform, hypochondriasis and pain disorder were deleted as separate diagnoses. Most map to somatic symptom disorder (≥ 1 distressing somatic symptom + excessive thoughts/feelings/behaviours, typically ≥ 6 months — note DSM no longer requires the symptom to be medically unexplained). Health anxiety without prominent somatic symptoms becomes illness anxiety disorder. Dysmorphophobia / body dysmorphic disorder leaves this group entirely in DSM-5 — it sits in the OCD & Related chapter (see the OCD section). (ICD-11 replaces the lot with a single "bodily distress disorder.")
Underlying organic disease (re-evaluate over time); depression/anxiety presenting somatically; panic disorder; factitious disorder and malingering (intentional). Manage with a single coordinating clinician, limited investigations, and a focus on function rather than symptom eradication.
Paste your licensed somatic-symptom and illness-anxiety-disorder criteria here.
Psychotic disorders F20–F29 · schizophrenia, schizotypal & delusional▾
Non-mood psychoses defined by delusions, hallucinations, disorganisation, or negative symptoms. Where psychosis occurs only within a mood episode, code the mood disorder with psychotic features instead. Residual codes F28 (other nonorganic psychosis) / F29 (unspecified) carry the leftovers.
↗ WHO block F20–F29 · DSM-5-TR: Schizophrenia Spectrum & Other Psychotic Disorders
SchizophreniaF20▾
ICD-10 view
Characteristic symptoms — delusions, hallucinations (esp. running commentary / third-person voices), thought interference/passivity, disorganised thinking/speech, catatonic or grossly disorganised behaviour, and negative symptoms (blunted affect, avolition) — present most of the time for ≥ 1 month, with impairment, not primarily explained by mood disorder, substances, or organic disease. Subtypes retained: paranoid, hebephrenic, catatonic, undifferentiated, residual, simple.
DSM-5-TR view — paraphrase (orientation; verbatim criteria belong in your licensed source)
A. ≥ 2 of the following for a significant portion of a 1-month active phase; ≥ 1 must be (1), (2) or (3):
- delusions (core positive)
- hallucinations (core positive)
- disorganised speech (core positive)
- grossly disorganised or catatonic behaviour
- negative symptoms (e.g. diminished expression, avolition)
B. Functioning (work/relationships/self-care) below prior level. C. Continuous signs ≥ 6 months, including the ≥ 1-month active phase (rest may be prodromal/residual). D. Schizoaffective and mood-with-psychosis excluded. E. Not attributable to a substance or another medical condition. (F: with an autism/communication-disorder history, diagnose only if prominent delusions/hallucinations ≥ 1 month.)
DSM-5 dropped the subtypes (paranoid, catatonic, …) and the first-rank weighting.
DSM-5-TR has a distinct schizophreniform disorder for the duration band ≥ 1 month but < 6 months (criterion-A symptoms, full functional recovery not required; provisional if recovery not yet observed) — a bridge between brief psychotic disorder (< 1 month) and schizophrenia (≥ 6 months). WHO ICD-10 has no separate code for it: such cases sit under F20.8 ("other schizophrenia" — schizophreniform NOS) or, when acute and shifting, F23.2 (acute schizophrenia-like psychotic disorder). (The US clinical modification ICD-10-CM adds a billable F20.81; the WHO version Romania codes from does not.)
ICD-10 treats catatonia as a schizophrenia subtype — F20.2 catatonic schizophrenia. DSM-5-TR instead handles catatonia as a cross-cutting specifier coded separately (F06.1, catatonia associated with another mental disorder), recognising it occurs in mood, autistic, and medical contexts too — not just schizophrenia. (ICD-11 goes further, making catatonia a standalone, cross-diagnostic entity; treatment differs — benzodiazepines/ECT, antipsychotics with caution.)
▸ Differs from ICD-10: the headline split is duration — DSM ≥ 6 months vs ICD-10 ≥ 1 month. DSM treats no single symptom as sufficient (needs ≥ 2, ≥ 1 positive), unlike ICD-10's first-rank emphasis where one can suffice; ICD-10 keeps subtypes DSM abolished.
Paste your licensed DSM-5-TR criterion wording and specifiers here; the view above is orientation only.
Exclude substance-induced psychosis, delirium, mood disorder with psychotic features, and organic causes (autoimmune/limbic encephalitis, temporal-lobe epilepsy, CNS lesion) — especially with rapid onset, fluctuating consciousness, or neurological signs. First-episode psychosis → prompt assessment, early-intervention pathway.
Add DSM 6-month logic, your first-episode workup, and organic-screen checklist.
Schizotypal disorderF21▾
Eccentric behaviour and anomalies of thinking and affect that resemble schizophrenia, but without definite or sustained psychotic symptoms: odd beliefs / magical thinking, suspiciousness, social withdrawal, constricted or inappropriate affect, unusual perceptual experiences, vague circumstantial speech.
Add your differentiation from schizoid/paranoid PD and from prodromal schizophrenia.
Persistent delusional disordersF22▾
ICD-10 view
A single delusion or a set of related delusions, usually persistent and sometimes lifelong, as the most conspicuous (often only) feature — without the hallucinations, thought disorder, or negative symptoms of schizophrenia. Duration ≥ 3 months. Personality and affect otherwise largely preserved.
DSM-5-TR view — paraphrase
A. ≥ 1 delusion lasting ≥ 1 month. B. Schizophrenia criterion A never met (hallucinations, if present, are not prominent and tie to the delusional theme). C. Function not markedly impaired apart from the delusion's direct effects; behaviour not bizarre. D. Any concurrent mood episodes are brief relative to the delusional periods. E. Not substance/medical, not better explained by another disorder.
Specifiers: erotomanic, grandiose, jealous, persecutory, somatic, mixed, unspecified; with bizarre content.
▸ Differs from ICD-10: duration — DSM 1 month vs ICD-10 3 months; otherwise closely aligned.
Paste your licensed wording and specifier set here.
Schizophrenia (F20), mood disorder with psychotic features, delusional presentations of OCD/body-dysmorphic disorder, organic and substance causes; assess dangerousness in persecutory/jealous types.
Acute & transient psychotic disordersF23▾
ICD-10 view
Acute onset (within ~2 weeks) of psychotic symptoms — often polymorphic and rapidly changing in type and intensity — frequently with associated acute stress, and typically full recovery within weeks to a few months. Subtyped by whether schizophrenia-type symptoms are present and whether an acute stressor preceded onset.
DSM-5-TR view — paraphrase
A. ≥ 1 of: delusions, hallucinations, disorganised speech, grossly disorganised or catatonic behaviour (≥ 1 must be one of the first three). B. Episode lasts ≥ 1 day but < 1 month, with eventual full return to premorbid function. C. Not better explained by mood-with-psychosis, schizoaffective, schizophrenia, or a substance/medical cause.
Specify: with / without marked stressor(s); with peripartum onset; with catatonia.
▸ Differs from ICD-10: not a tidy one-to-one map. DSM's brief psychotic disorder caps at < 1 month; ICD-10 F23 allows a longer transient course (weeks–months) and foregrounds the polymorphic, shifting picture and stress association. Longer cases route to schizophreniform / schizophrenia in DSM.
Paste your licensed wording here.
Induced delusional disorderF24▾
A delusional system shared by two (or more) people in a close emotional relationship (folie à deux): only one has a genuine psychotic disorder, and the induced delusions in the other(s) usually resolve once the pair is separated.
Add management note: separation, treat the primary case, reassess the induced party.
Schizoaffective disordersF25▾
↗ F25 (.0 manic · .1 depressive · .2 mixed type)
ICD-10 view
Both definite schizophrenic and definite mood (manic or depressive) symptoms are prominent within the same episode, simultaneously or within a few days of each other — so the episode fits neither schizophrenia nor a mood disorder alone. Typed by the mood pole: manic, depressive, or mixed.
DSM-5-TR view — paraphrase
A. An uninterrupted illness period with a major mood episode concurrent with schizophrenia criterion A. B. Delusions or hallucinations for ≥ 2 weeks without a major mood episode at some point in the lifetime of the illness (the discriminator). C. Mood-episode symptoms are present for the majority of the total illness duration. D. Not substance/medical. Type: bipolar or depressive.
▸ Differs from ICD-10: DSM hinges on its longitudinal Criterion B — ≥ 2 weeks of psychosis without mood — which ICD-10 doesn't formalise; ICD-10 reads more cross-sectionally (both prominent in the same episode). Practical upshot: DSM schizoaffective is a narrower, course-based label.
Paste your licensed wording here.
Schizophrenia with post-psychotic depression, mood disorder with psychotic features, schizophrenia plus comorbid mood disorder. Longitudinal history (timing of psychosis vs mood) is what makes the call.
Neurodevelopmental disorders F80–F90 · developmental + hyperkinetic▾
Early-onset impairments tied to CNS maturation — speech/language, scholastic skills, motor coordination, the autism spectrum, and the hyperkinetic (ADHD) disorders. F83 (mixed specific developmental) and the F88/F89 residuals fold here; F90 hyperkinetic lives in this section, with the rest of F90–F98 in the Conduct & childhood-onset section below.
↗ WHO block F80–F89 · ↗ WHO F90 · DSM-5-TR: Neurodevelopmental Disorders
Speech & language disordersF80▾
Language acquisition disturbed from the earliest stages, not attributable to neurological/sensory deficit, intellectual disability, or environment. F80.0 articulation (speech-sound use below mental age, normal language); F80.1 expressive (use of spoken language below mental age, comprehension normal); F80.2 receptive (understanding below mental age, almost always with expressive impairment too); F80.3 Landau-Kleffner (acquired aphasia + EEG paroxysms/seizures, onset 3–7 y).
DSM-5 groups these as Communication Disorders — language disorder, speech sound disorder, childhood-onset fluency disorder (stuttering — note ICD-10 files stuttering separately at F98.5), and social (pragmatic) communication disorder (a DSM-5 addition with no ICD-10 equivalent).
Exclude hearing loss (H90–H91), intellectual disability (F70–F79), autism (F84), and elective/selective mutism (F94.0). Acquired aphasia routes to R47.0 unless the Landau-Kleffner picture applies.
Paste your licensed Communication Disorders criteria here.
Scholastic skills disordersF81▾
Skill acquisition disturbed from early development, not explained by lack of opportunity, intellectual disability, or acquired brain injury. F81.0 reading disorder (developmental dyslexia — impaired reading accuracy/comprehension, spelling difficulties common); F81.1 spelling disorder (without a reading disorder); F81.2 arithmetical disorder (developmental dyscalculia/acalculia, basic computation rather than abstract maths); F81.3 mixed (arithmetic + reading/spelling both impaired).
DSM-5 merges the lot into one specific learning disorder with coded specifiers (with impairment in reading / written expression / mathematics) and severity — replacing ICD-10's separate reading/spelling/arithmetic categories with a single dimensional diagnosis.
Paste your licensed specific learning disorder criteria and specifiers here.
Motor function disorderF82▾
↗ F82 (no sub-codes — developmental coordination disorder / dyspraxia)
Serious impairment of motor coordination development not explained by intellectual disability or a specific congenital/acquired neurological disorder, often with neurodevelopmental "soft signs". Includes clumsy child syndrome and developmental dyspraxia / coordination disorder.
DSM-5 keeps this as developmental coordination disorder within the motor-disorders group of the Neurodevelopmental chapter (alongside stereotypic movement disorder and the tic disorders).
Paste your licensed developmental coordination disorder criteria here.
Autism & pervasive developmental disordersF84▾
ICD-10 view
Early-onset qualitative impairments in reciprocal social interaction and communication, plus a restricted, stereotyped, repetitive repertoire of interests/activities, pervasive across situations. ICD-10 retains distinct subtypes: F84.0 childhood autism (onset before age 3, all three domains affected), F84.1 atypical autism (later onset or sub-threshold in one/two domains), F84.2 Rett (girls; regression with hand-wringing stereotypies and head-growth deceleration), F84.3 disintegrative disorder (Heller — normal development then marked regression), and F84.5 Asperger (autistic social/repetitive features without general language or cognitive delay).
DSM-5-TR view — paraphrase (orientation; verbatim criteria belong in your licensed source)
A. Persistent deficits in social communication and interaction across contexts — social-emotional reciprocity, nonverbal communication, and developing/maintaining relationships (all three).
B. Restricted, repetitive patterns of behaviour/interests/activities — ≥ 2 of: stereotyped/repetitive movements or speech; insistence on sameness/routines; highly restricted fixated interests; hyper- or hypo-reactivity to sensory input.
C–D. Symptoms present in early development and cause clinically significant impairment.
Coded with severity levels 1–3 (support needs) and specifiers (with/without intellectual or language impairment).
▸ Differs from ICD-10: DSM-5 collapsed every subtype into one ASD — Asperger, atypical autism and disintegrative disorder are gone as labels, replaced by a single spectrum with severity tiers; the old triad became a dyad (social-communication + restricted/repetitive), with sensory reactivity added. Rett syndrome was removed from the classification entirely (now a genetic/medical diagnosis). DSM also added social (pragmatic) communication disorder for social-communication deficits without the restricted/repetitive component.
Paste your licensed ASD criteria, severity levels, and specifiers here; the view above is orientation only.
Diagnosis rests on developmental history + cross-setting observation; structured tools (e.g. ADOS/ADI-R) support but don't replace clinical assessment. Screen comorbidity (intellectual disability — code F70–F79 additionally; ADHD; anxiety; epilepsy). Differentiate from intellectual disability without ASD, selective mutism, and receptive language disorder.
Hyperkinetic disorders (ADHD)F90▾
ICD-10 view
Early-onset (usually before age 5), cross-situational combination of impaired attention and overactivity/impulsivity beyond the developmental norm, causing impairment. F90.0 is the core disturbance of activity and attention; F90.1 applies when the full conduct-disorder criteria are also met (hyperkinetic conduct disorder). ICD-10 requires both inattention and hyperactivity — there is no inattentive-only category (inattention without hyperactivity is coded F98.8).
DSM-5-TR view — paraphrase (orientation; verbatim criteria belong in your licensed source)
A. A persistent pattern of inattention and/or hyperactivity-impulsivity interfering with functioning — ≥ 6 symptoms (≥ 5 if age ≥ 17) from either the inattention list or the hyperactivity-impulsivity list, for ≥ 6 months.
B–E. Several symptoms before age 12; present in ≥ 2 settings; clear impairment; not better explained by another disorder.
Presentations: predominantly inattentive, predominantly hyperactive-impulsive, or combined; with severity.
▸ Differs from ICD-10: DSM ADHD is broader — it allows an inattentive-only presentation that ICD-10 hyperkinetic disorder does not recognise, raised the onset age to before 12 (ICD-10 emphasises onset before 5), and does not require both symptom clusters together. ICD-10's F90.1 (with conduct disorder) has no direct DSM equivalent — DSM codes ADHD and conduct disorder as comorbid diagnoses.
Paste your licensed ADHD criteria, presentations, and specifiers here; the view above is orientation only.
Adult ADHD diagnosis rests on developmental history + current cross-setting impairment; rating scales support, not replace, assessment. Screen common comorbidities (mood, anxiety, substance use). Confirm stimulant scheduling/availability in Romania before planning treatment.
Add your adult-ADHD criteria (often DSM-framed), rating scales, and Romanian stimulant availability.
Intellectual disability F70–F79 · developmental▾
Arrested or incomplete development of the mind affecting cognitive, language, motor and social abilities, manifest during the developmental period. F78 (other) and F79 (unspecified) fold here. ICD-10's legacy term is "mental retardation"; current usage is "intellectual disability".
↗ WHO block F70–F79 · DSM-5-TR: Intellectual Developmental Disorder (Neurodevelopmental chapter)
Intellectual disability (severity grades)F70–F73▾
ICD-10 view
Severity set by standardised IQ (supplemented by social-adaptation scales and clinical judgement; diagnose on current functioning):
F70 Mild — IQ ≈ 50–69 (adult mental age 9 to <12 y); some schooling difficulty, many live and work independently. F71 Moderate — IQ ≈ 35–49 (MA 6 to <9 y); marked childhood delay, partial self-care independence, community support needed. F72 Severe — IQ ≈ 20–34 (MA 3 to <6 y); continuous support. F73 Profound — IQ < 20 (MA < 3 y); severe limitation in self-care, continence, communication, mobility.
A fourth character grades behavioural impairment: .0 none/minimal · .1 significant, needing attention/treatment · .8 other · .9 not mentioned.
DSM-5-TR view — paraphrase (orientation; verbatim criteria belong in your licensed source)
A. Deficits in intellectual functions (reasoning, problem-solving, abstract thinking, judgement, learning) confirmed by clinical assessment and individualised testing.
B. Deficits in adaptive functioning failing developmental/sociocultural standards for independence and social responsibility, across conceptual, social and practical domains.
C. Onset during the developmental period.
Severity (mild / moderate / severe / profound) is set by adaptive functioning, not IQ score.
▸ Differs from ICD-10: DSM determines severity by adaptive functioning rather than IQ band, drops the "mental retardation" term, and folds the ICD-10 behavioural-impairment modifier into the broader adaptive picture. The label is intellectual disability (intellectual developmental disorder).
Paste your licensed intellectual disability criteria and adaptive-domain severity descriptors here; the view above is orientation only.
Distinguish from specific learning disorder (F81 — circumscribed, normal global intelligence), autism (F84 — can co-occur; code additionally), and acquired cognitive decline (dementia, F00–F03). ICD-10 invites an additional code for associated autism, epilepsy, conduct or physical disorder.
Conduct & childhood-onset disorders F91–F98 · onset in childhood/adolescence▾
Behavioural and emotional disorders usually beginning in childhood or adolescence — conduct, mixed conduct/emotion, childhood emotional disorders, social-functioning disorders, tics, and the F98 miscellany (enuresis, encopresis, feeding, stuttering). F90 hyperkinetic/ADHD sits in the Neurodevelopmental section above — cross-referenced, not duplicated. F93.3 sibling rivalry and the F9x.8/.9 residuals fold into their cards.
↗ WHO block F90–F98 · DSM-5-TR: Disruptive, Impulse-Control & Conduct Disorders; Anxiety; Elimination; Neurodevelopmental (tics)
Conduct disorders (incl. ODD)F91▾
ICD-10 view
A repetitive, persistent pattern (≥ 6 months) of dissocial, aggressive or defiant conduct amounting to major violations of age-appropriate social expectations — beyond ordinary mischief or rebelliousness. Examples: fighting/bullying, cruelty to people or animals, destructiveness, fire-setting, stealing, lying, truancy, running away, severe tantrums. Subtypes by social context: F91.0 confined to the family, F91.1 unsocialized (poor peer relationships), F91.2 socialized (within a peer/gang group). F91.3 oppositional defiant disorder — markedly defiant/disobedient/disruptive behaviour in younger children without serious dissocial or aggressive acts, nested here under conduct disorder.
DSM-5-TR view — paraphrase (orientation; verbatim criteria belong in your licensed source)
Conduct disorder. A repetitive pattern violating others' basic rights or major age-appropriate norms — ≥ 3 of 15 behaviours across aggression to people/animals, destruction of property, deceitfulness/theft, and serious rule violations, over 12 months. Childhood-onset vs adolescent-onset; "with limited prosocial emotions" specifier.
Oppositional defiant disorder. A separate diagnosis — a pattern of angry/irritable mood, argumentative/defiant behaviour, and vindictiveness (≥ 4 symptoms, ≥ 6 months).
▸ Differs from ICD-10: DSM places these in Disruptive, Impulse-Control & Conduct Disorders and treats ODD as its own disorder, not a subtype of conduct disorder; it adds the "limited prosocial emotions" (callous-unemotional) specifier and onset typing. ICD-10's context-based F91.0–.2 subtyping has no DSM analogue.
Paste your licensed conduct disorder and ODD criteria and specifiers here; the view above is orientation only.
Exclude mood/affective disorder, ADHD (F90 — frequently comorbid; F90.1 codes the combination in ICD-10), autism, and adjustment reactions. When emotional symptoms co-occur prominently, see F92 mixed.
Mixed conduct & emotional disordersF92▾
↗ F92 (.0 depressive conduct disorder · .8 other mixed · .9 unspecified)
Persistent aggressive/dissocial/defiant behaviour combined with marked emotional symptoms — the criteria for both a conduct disorder (F91) and a childhood emotional disorder (F93), an adult-type neurotic disorder (F40–F48), or a mood disorder (F30–F39) must be met. F92.0 requires conduct disorder + marked depression; F92.8 conduct disorder + anxiety/obsessions/phobias/etc.
DSM-5 has no single "mixed conduct and emotions" category. The same clinical picture is captured by coding the conduct disorder and the co-occurring depressive or anxiety disorder as separate comorbid diagnoses.
Paste your licensed criteria for the relevant comorbid conduct + mood/anxiety diagnoses here.
Childhood emotional disordersF93▾
Mainly exaggerations of normal developmental trends rather than qualitatively abnormal phenomena — developmental appropriateness is the key feature distinguishing these from the adult neurotic disorders (F40–F48). F93.0 separation anxiety (fear of separation, abnormal in degree/persistence, onset in early childhood); F93.1 phobic anxiety (developmentally-typical fears, abnormal in degree); F93.2 social anxiety (wariness of strangers / avoidant disorder of childhood); F93.3 sibling rivalry.
DSM-5 moved separation anxiety disorder into the main Anxiety Disorders chapter — no longer restricted to childhood onset (adults can be diagnosed). The childhood phobic and social-anxiety presentations map onto the general specific-phobia and social-anxiety disorders. See also the Anxiety & phobic section's "where it lives" note on F41 for how ICD-10 routes adult-type anxiety.
Paste your licensed separation-anxiety and related criteria here.
Social functioning disordersF94▾
Abnormalities of social functioning beginning in the developmental period but — unlike the pervasive developmental disorders — not pervading all areas; environmental privation often plays a causal role. F94.0 elective (selective) mutism — emotionally-determined selectivity in speaking (competent in some settings, silent in others), with social anxiety/withdrawal. F94.1 reactive attachment disorder (fearful/hypervigilant, poor peer interaction, following neglect/abuse) and F94.2 disinhibited attachment disorder (diffuse, indiscriminately friendly attachment).
DSM-5 moves selective mutism into the Anxiety Disorders chapter, and places the two attachment disorders — reactive attachment disorder and disinhibited social engagement disorder — in the Trauma- & Stressor-Related Disorders chapter, reflecting their basis in social neglect.
Paste your licensed selective-mutism and attachment-disorder criteria here.
Tic disorders (incl. Tourette)F95▾
Tics — involuntary, rapid, recurrent, nonrhythmic motor movements or vocalisations, suppressible for periods, worsened by stress, absent in sleep. F95.0 transient (≤ 12 months); F95.1 chronic motor OR vocal (one type, > 1 year); F95.2 Tourette (multiple motor tics + ≥ 1 vocal tic, not necessarily concurrent; may include coprolalia/copropraxia; persists into adult life).
DSM-5 places tic disorders in the Neurodevelopmental chapter (motor disorders) with closely parallel categories — provisional, persistent (chronic) motor or vocal, and Tourette's disorder — keeping the > 1-year and onset-before-18 framing.
Distinguish from stereotyped movement disorder (F98.4), chorea/dystonia and other organic movement disorders (G20–G25), and OCD (frequently comorbid). Trichotillomania is coded F63.3, not here.
Paste your licensed tic-disorder criteria here.
Other childhood-onset disordersF98▾
A heterogeneous miscellany sharing childhood onset. Elimination: F98.0 nonorganic enuresis (involuntary voiding, abnormal for mental age, no neurological/structural cause), F98.1 nonorganic encopresis (passage of faeces in inappropriate places). Feeding: F98.2 feeding disorder of infancy/childhood (food refusal/faddiness, may include rumination), F98.3 pica (eating non-nutritive substances). Movement/speech: F98.4 stereotyped movement disorder (rocking, head-banging, self-injurious), F98.5 stuttering/stammering, F98.6 cluttering. F98.8 sweeps up nail-biting, thumb-sucking, nose-picking, and attention deficit disorder without hyperactivity.
DSM-5 scatters these: enuresis and encopresis become a dedicated Elimination Disorders chapter; feeding disorder of infancy maps largely onto ARFID and rumination disorder lands in Feeding & Eating (see that section); pica likewise; stereotypic movement disorder and stuttering (childhood-onset fluency disorder) move to the Neurodevelopmental chapter. Note ICD-10's F98.8 "attention deficit disorder without hyperactivity" is the inattentive-only presentation that DSM ADHD recognises but ICD-10 hyperkinetic disorder (F90) does not.
Paste your licensed elimination / feeding / fluency / stereotypic-movement criteria here.
Personality & adult behaviour F60–F69▾
Deeply ingrained, enduring patterns of inner experience and behaviour, plus the adult behavioural syndromes ICD-10 files alongside them (impulse, sexual, gender, factitious). Residual code F69 folded here.
↗ WHO block F60–F69 · DSM-5-TR: Personality Disorders (+ Paraphilic, Gender Dysphoria, Disruptive/Impulse-Control, and Somatic-Symptom chapters)
Specific personality disordersF60▾
ICD-10 view
Enduring, pervasive, inflexible patterns of inner experience and behaviour deviating markedly from cultural expectation, stable and long-standing with onset in adolescence/early adulthood, causing distress or impairment. ICD-10 specific types: paranoid (.0), schizoid (.1), dissocial (.2), emotionally unstable (.3 — impulsive .30 / borderline .31), histrionic (.4), anankastic (.5), anxious/avoidant (.6), dependent (.7).
DSM-5-TR view — paraphrase (orientation; verbatim criteria belong in your licensed source)
A general PD definition (enduring, pervasive, inflexible pattern across cognition, affect, interpersonal functioning, impulse control; stable; impairing), then 10 specific types grouped into three clusters: A (odd/eccentric: paranoid, schizoid, schizotypal), B (dramatic/erratic: antisocial, borderline, histrionic, narcissistic), C (anxious/fearful: avoidant, dependent, obsessive-compulsive). Section III adds an Alternative Model (level-of-functioning + five pathological trait domains).
▸ Differs from ICD-10: DSM includes narcissistic and schizotypal PDs (ICD-10 codes schizotypal up in F21, not here, and has no narcissistic type). DSM's antisocial ≈ ICD-10 dissocial; obsessive-compulsive PD ≈ anankastic; borderline ≈ emotionally-unstable, borderline type. ICD-11 abandons all categories for a dimensional severity-plus-traits system.
Paste your licensed PD definitions and the Section III Alternative Model traits here.
Distinguish trait from state (mood/psychotic episode), and from organic personality change (F07 — see Organic section). EUPD/borderline: structured psychological therapy (DBT, MBT) is first-line; medication is adjunctive and targets comorbidity, not the disorder itself.
Add cluster mapping, ICD-11 trait domains, and your EUPD management approach.
Mixed & other personality disordersF61▾
For PDs that don't fit one specific F60 type — mixed presentations with features of several, or troublesome personality changes secondary to a coexisting affective/anxiety disorder. Where it lives in DSM: roughly "personality disorder — mixed / other specified / unspecified." ICD-11's dimensional model dissolves this category by design.
Enduring personality change (non-organic)F62▾
↗ F62 (.0 after catastrophic experience · .1 after psychiatric illness)
A definite, enduring change in personality acquired in someone with no prior PD, following catastrophic/prolonged stress (F62.0) — e.g. captivity, torture, disaster — or a severe psychiatric illness (F62.1). Distinct from the lifelong patterns of F60 (no organic cause, so not F07).
F62.0 is the historical precursor of ICD-11 complex PTSD (see the Stress section), which superseded it. DSM-5 has no direct equivalent — such presentations fold into its broadened PTSD. (Placed here, in the personality block, because that is where WHO ICD-10 codes it.)
Habit & impulse disordersF63▾
↗ F63 (.0 pathological gambling · .1 pyromania · .2 kleptomania · .3 trichotillomania)
Repeated failure to resist an impulse to perform an act harmful to self or others, with rising tension before and relief/gratification after: pathological gambling (.0), pyromania (.1), kleptomania (.2), trichotillomania (.3).
DSM scatters these: gambling disorder moved to Substance-Related & Addictive Disorders (a behavioural addiction; ICD-11 agrees); trichotillomania moved to the OCD & Related chapter (see OCD); pyromania and kleptomania sit in DSM's Disruptive, Impulse-Control & Conduct chapter, which also holds intermittent explosive disorder (no neat ICD-10 home).
Gender identity disordersF64▾
↗ F64 (.0 transsexualism · .1 dual-role transvestism · .2 gender identity disorder of childhood)
ICD-10 places gender-identity diagnoses in this block under the now-superseded terms transsexualism (F64.0), dual-role transvestism (F64.1), and gender identity disorder of childhood (F64.2). These ICD-10 labels are stated here as a factual record of the classification Romania still codes against.
ICD-11 removed gender-identity diagnoses from the mental-disorders chapter entirely. It renamed them gender incongruence (of adolescence/adulthood; of childhood) and moved them to a new chapter, Conditions related to sexual health — explicitly to reflect that trans and gender-diverse identities are not mental illness and to reduce stigma, while retaining a code to preserve access to healthcare. ICD-11 requires no distress or dysfunction. DSM-5 took a middle path: it renamed gender identity disorder to gender dysphoria and kept it in the manual, but reframed the diagnosis around clinically significant distress/impairment — so gender variance alone is explicitly not a disorder. Use current, person-centred terminology in practice.
Paste your local gender-care pathway and the current ICD-11 / DSM-5-TR terminology you use clinically.
Disorders of sexual preference (paraphilic)F65▾
ICD-10 view
ICD-10 lists named subtypes under F65 disorders of sexual preference: fetishism (.0), fetishistic transvestism (.1), exhibitionism (.2), voyeurism (.3), paedophilia (.4), sadomasochism (.5), multiple/other (.6/.8). ICD-10 does not formalise the paraphilia-vs-disorder distinction as sharply as later systems.
DSM-5-TR view — paraphrase (orientation; verbatim criteria belong in your licensed source)
Explicit in DSM-5-TR (and ICD-11): a paraphilia (an atypical sexual interest) is not in itself a disorder. A paraphilic disorder additionally requires either clinically significant distress/impairment to the individual, or that the interest is acted on with a non-consenting person (or otherwise entails marked risk of harm to others). DSM recasts each ICD subtype as a paraphilia vs paraphilic-disorder pair and splits sadomasochism into sexual sadism and sexual masochism disorders.
▸ Differs from ICD-10: the distress/impairment-or-harm threshold is formalised in DSM/ICD-11 but only implicit in ICD-10. ICD-11 restructures the grouping around consent, distress and risk of harm, de-listing categories that merely describe consensual atypical behaviour between adults — a deliberate de-pathologising shift.
Paste your licensed paraphilic-disorder criteria here.
Risk framing: where the interest involves non-consenting others, use a structured risk assessment — history of acting on urges, access to potential victims, insight, treatment engagement. Differentials: sexual behaviour better explained by a manic or psychotic episode, intoxication, a neurocognitive disorder or other disinhibition, intellectual disability, or ego-dystonic intrusive sexual thoughts of OCD (unwanted, not desired). Duty considerations: confidentiality is not absolute — a credible risk of serious harm to an identifiable other (especially a child) may engage safeguarding/disclosure duties; know your jurisdiction's reporting law. Paedophilic disorder is handled strictly at the level of diagnosis and risk management: attraction is not the same as offending, not everyone who offends against children has it, and recognised assessment/treatment pathways exist.
Psychological therapy is first-line — CBT on offence-supportive cognitions, self-regulation, victim awareness. Pharmacology is adjunctive where distress or risk is high: SSRIs (milder end) and, for high-risk cases, anti-androgen / testosterone-lowering agents (cyproterone acetate; GnRH analogues) under specialist forensic/endocrine governance and consent. See forensic-psychiatry sources and your local pathway.
Add your structured risk-assessment tool, safeguarding/disclosure thresholds, and local forensic referral pathway.
Other disorders of adult personality & behaviourF68▾
↗ F68 (.0 elaboration of symptoms for psychological reasons · .1 factitious disorder)
Includes factitious disorder (F68.1) — intentional production or feigning of symptoms/disabilities (physical or psychological) to assume the sick role, with no external incentive (historically "Munchausen"). Distinct from malingering (Z76.5), where the motive is external gain.
DSM-5 moves factitious disorder into the Somatic Symptom & Related Disorders chapter (imposed on self, or on another). Malingering is not a mental disorder in either system.
Psychoactive substance use F10–F19▾
Mental and behavioural disorders caused by psychoactive substances — one 3-character code per substance class, each carrying the same clinical-state grid below.
↗ WHO block F10–F19 · DSM-5-TR: Substance-Related & Addictive Disorders
Every substance code F10–F19 takes the same fourth-character qualifier for clinical state: .0 acute intoxication · .1 harmful use · .2 dependence syndrome · .3 withdrawal state · .4 withdrawal with delirium · .5 psychotic disorder · .6 amnesic syndrome · .7 residual / late-onset psychotic disorder · .8 other · .9 unspecified. Dependence syndrome = ≥ 3 of the following over the prior year: strong desire/compulsion, impaired control, tolerance, a physiological withdrawal state, salience of use over other activities, and persistence despite clear harm.
Cross-cutting red flag: anticipate withdrawal. Alcohol and sedative withdrawal can be fatal (seizures, delirium tremens). Screen for Wernicke's and give thiamine before glucose in at-risk alcohol use. The alcohol amnesic (Korsakoff) syndrome codes to F10.6.
AlcoholF10▾
↗ F10 (.0–.9 grid as above; .4 withdrawal with delirium = DTs; .6 amnesic = Korsakoff)
ICD-10 view
Applies the shared grid to alcohol. Harmful use (F10.1): a pattern causing physical/mental harm without dependence. Dependence syndrome (F10.2): ≥ 3 dependence features over the prior year. Withdrawal (F10.3) ranges to delirium tremens (F10.4); alcohol amnesic syndrome / Korsakoff = F10.6.
DSM-5-TR view — paraphrase (orientation; verbatim criteria belong in your licensed source)
A single disorder requiring ≥ 2 of 11 criteria in 12 months, across impaired control (using more/longer than intended, failed cut-down, craving, time spent), social impairment, risky use, and pharmacological features (tolerance, withdrawal). Severity: mild 2–3 · moderate 4–5 · severe 6+. Intoxication and withdrawal are coded as separate substance-induced states.
▸ Differs from ICD-10: DSM collapses harmful use + dependence into one graded disorder instead of two categories, drops the legal-problems criterion, and adds craving.
Paste your licensed AUD criteria here.
Distinguish from mood/anxiety disorders driving use. Withdrawal can be lethal — assess with a structured scale, treat with a benzodiazepine regimen, and give parenteral thiamine to prevent Wernicke's. Tools: AUDIT, breath/blood alcohol.
Add your local alcohol-withdrawal and relapse-prevention protocols (acamprosate, naltrexone, disulfiram).
OpioidsF11▾
Heroin, morphine, methadone, prescription opioids, fentanyl. Overdose (respiratory depression) is a medical emergency — naloxone. Withdrawal is intensely unpleasant but rarely fatal in the otherwise healthy. = DSM opioid use disorder; substitution therapy (methadone, buprenorphine) is mainstay.
CannabinoidsF12▾
Cannabis/THC. Associated with anxiety, psychotic symptoms, and a dependence syndrome. Cannabis withdrawal was newly recognised in DSM-5 (not separately operationalised in ICD-10).
Sedatives or hypnoticsF13▾
Benzodiazepines, barbiturates, "Z-drugs". Like alcohol, withdrawal can be life-threatening (seizures) — taper, never abrupt cessation in dependence.
CocaineF14▾
ICD-10 gives cocaine its own code, separate from other stimulants. Intoxication can cause agitation, paranoia, cardiovascular crisis; a depressive "crash" follows.
Other stimulants (incl. caffeine)F15▾
Amphetamines, methamphetamine, MDMA, and caffeine. Stimulant psychosis can mimic schizophrenia. (DSM groups amphetamine-type and cocaine under "stimulant use disorder", and added caffeine withdrawal.)
HallucinogensF16▾
LSD, psilocybin, PCP and related. Acute "bad trips", and persisting perceptual phenomena (flashbacks/HPPD) can occur. Physiological dependence is limited.
TobaccoF17▾
Nicotine dependence and withdrawal. DSM-5 aligned tobacco-use-disorder criteria with the other substances (DSM-IV had treated nicotine differently). Manage with NRT, varenicline, bupropion + behavioural support.
Volatile solventsF18▾
Inhalants — glue, aerosols, gases. Predominantly an adolescent pattern; risk of "sudden sniffing death" (arrhythmia) and organ toxicity. = DSM inhalant use disorder.
Multiple / other psychoactive substancesF19▾
Used when several substances are taken or the agent is unknown. (DSM-5 dropped the older "polysubstance dependence" construct — code each substance's use disorder separately where identifiable.)
Organic / neurocognitive disorders F00–F09 · organic▾
Mental disorders with a demonstrable cerebral or systemic physical cause — dementia, delirium, amnesia, and the organic mimics of psychiatric syndromes. Residual code F09 folded here.
↗ WHO block F00–F09 · DSM-5-TR: Neurocognitive Disorders (+ "due to another medical condition" entries scattered across chapters)
Dementia in Alzheimer's diseaseF00▾
↗ F00 (early-onset .0 · late-onset .1 · atypical/mixed .2)
Insidious, progressive decline in memory and other cognitive domains in clear consciousness, with no other identifiable cause — the prototype dementia. ICD-10 subtypes by age of onset.
= Major (or mild) neurocognitive disorder due to Alzheimer's disease. Cholinesterase inhibitors (donepezil, rivastigmine, galantamine) and memantine are symptomatic; confirm clinical detail in your licensed source.
Antipsychotics in dementia carry increased stroke and mortality risk — reserve for severe distress/risk, lowest dose, shortest time, documented review. Always exclude delirium first.
Vascular dementiaF01▾
↗ F01 (incl. multi-infarct .1)
Cognitive decline attributable to cerebrovascular disease, classically with stepwise deterioration, patchy deficits, and focal neurological signs. = DSM major/mild NCD due to vascular disease.
Dementia in other diseasesF02▾
↗ F02 (.0 Pick · .1 Creutzfeldt–Jakob · .2 Huntington · .3 Parkinson · .4 HIV)
Dementia occurring as part of another named disease — Pick (frontotemporal), Creutzfeldt–Jakob, Huntington, Parkinson, HIV, and others. Lewy body and frontotemporal dementias map here in WHO ICD-10 (they have dedicated major/mild NCD subtypes in DSM-5).
Unspecified dementiaF03▾
Dementia where the aetiology is not yet established. = DSM major/mild NCD due to unknown aetiology (DSM codes severity + behavioural-disturbance status here).
Organic amnesic syndromeF04▾
↗ F04 (not alcohol/substance-induced)
Prominent impairment of recent and remote memory with preserved immediate recall and otherwise intact cognition/consciousness — out of proportion to any other deficit. = DSM amnestic presentation / major NCD. The alcohol-induced (Korsakoff) form codes to F10.6 in the substance block, not here.
DeliriumF05▾
↗ F05 (not alcohol/substance-induced; .1 superimposed on dementia)
ICD-10 view
An acute, fluctuating disturbance of consciousness and attention, with global cognitive impairment, altered psychomotor activity, disturbed sleep–wake cycle, and an emotional component — developing over hours to days with an identifiable physical cause. A medical emergency. F05.1 = delirium superimposed on dementia.
DSM-5-TR view — paraphrase (orientation; verbatim criteria belong in your licensed source)
A. Disturbance in attention and awareness. B. Develops acutely (hours–days), a change from baseline, fluctuating over the day. C. An additional cognitive disturbance (memory, disorientation, language, perception). D. Not better explained by another NCD and not in a coma. E. Evidence of a medical cause, substance, or multiple aetiologies. Specify hyperactive / hypoactive / mixed.
▸ Differs from ICD-10: closely aligned. DSM foregrounds the attention/awareness disturbance as the core feature and offers explicit psychomotor specifiers; substance-induced delirium is coded in the substance chapters in both systems (ICD-10 → F1x.4).
Paste your licensed delirium criteria here.
Always exclude delirium before diagnosing a primary psychiatric disorder in an acutely disturbed patient — hypoxia, sepsis, metabolic derangement, intoxication/withdrawal, intracranial events. Investigate and treat the cause; antipsychotics are symptomatic only.
Other organic mental disordersF06▾
Psychiatric syndromes that phenocopy "functional" disorders but arise from brain damage/dysfunction or systemic disease: organic hallucinosis (.0), organic catatonic disorder (.1), organic delusional/schizophrenia-like (.2), organic mood (.3), organic anxiety (.4), organic dissociative (.5), organic emotionally labile/asthenic (.6), and mild cognitive disorder (.7).
DSM disperses these as "… due to another medical condition" diagnoses within the matching chapters (e.g. psychotic disorder due to another medical condition, mood disorder due to another medical condition). F06.1 organic catatonic ≈ DSM catatonia due to another medical condition / catatonia specifier — cross-referenced from the Psychotic section. F06.7 mild cognitive disorder roughly parallels DSM mild neurocognitive disorder.
Paste the relevant "due to another medical condition" criteria here.
Organic personality & behavioural disordersF07▾
↗ F07 (.0 organic personality · .1 postencephalitic · .2 postconcussional)
Persistent change in personality or behaviour following brain disease, damage, or dysfunction — altered emotional expression, impulse control, and social conduct (e.g. frontal-lobe disinhibition). Includes postencephalitic (.1) and postconcussional (.2) syndromes.
= DSM personality change due to another medical condition. Distinguish from a primary personality disorder (lifelong pattern, no organic cause) — see the Personality & adult-behaviour section.
Behavioural / physiological disorders F50–F59 · eating, sleep, sexual, puerperal▾
Behavioural syndromes tied to physiological disturbance or physical factors — eating, nonorganic sleep, nonorganic sexual dysfunction, postpartum, and psychological factors affecting physical illness. F55 (abuse of non-dependence-producing substances — laxatives, analgesics, vitamins, steroids) and the F59 residual fold in here; F55 is distinct from F10–F19 because dependence/withdrawal do not develop.
↗ WHO block F50–F59 · DSM-5-TR: Feeding & Eating; Sleep–Wake; Sexual Dysfunctions (separate chapters)
Eating disordersF50▾
ICD-10 view
Anorexia nervosa (F50.0): deliberate weight loss / maintained low body weight (ICD-10 uses BMI ≤ 17.5 as a guide), dread of fatness as an intrusive overvalued idea, with endocrine effects (amenorrhoea, loss of sexual interest). Atypical anorexia (F50.1): some features absent (e.g. amenorrhoea or dread of fatness) but the core weight-reducing behaviour present. Bulimia nervosa (F50.2): recurrent binge–compensatory cycles with overvaluation of weight/shape, usually at near-normal weight. F50.4–.5 cover psychogenic overeating and vomiting tied to other psychological disturbance; F50.8 includes pica in adults.
DSM-5-TR view — paraphrase (orientation; verbatim criteria belong in your licensed source)
Anorexia nervosa. Restriction of intake → significantly low weight; intense fear of weight gain or persistent behaviour interfering with weight gain; disturbed experience of body weight/shape. Restricting vs binge–purge subtype; severity by BMI.
Bulimia nervosa. Recurrent binge eating + recurrent inappropriate compensatory behaviour, on average ≥ 1×/week for 3 months; self-evaluation unduly influenced by shape/weight; not occurring exclusively during anorexia.
Binge-eating disorder. Recurrent binges with marked distress and no regular compensatory behaviour, ≥ 1×/week for 3 months — a full DSM diagnosis with no ICD-10 code.
ARFID. Avoidant/restrictive food intake (sensory aversion, low interest, fear of aversive consequences) without body-image disturbance — also DSM-5+ only.
▸ Differs from ICD-10: DSM dropped amenorrhoea from anorexia and removed the explicit BMI floor (uses "significantly low" + severity tiers); adds binge-eating disorder and ARFID as standalone diagnoses that ICD-10 cannot code (BED maps loosely to F50.4 / F50.8; ICD-11 adds both formally).
Paste your licensed anorexia / bulimia / BED / ARFID criteria and severity specifiers here; the view above is orientation only.
Eating disorders carry the highest mortality in psychiatry. Watch bradycardia, hypotension, electrolyte derangement, and refeeding syndrome (hypophosphataemia) on re-nutrition. Manage medical risk first; use a risk framework (e.g. MEED / local protocol) and involve medicine early.
Add your refeeding and medical-monitoring protocol (e.g. MEED thresholds, electrolyte schedule).
Nonorganic sleep disordersF51▾
Sleep disturbance where emotional causes are the primary factor and no identifiable physical cause applies. Dyssomnias — F51.0 insomnia (unsatisfactory quantity/quality, persisting), F51.1 hypersomnia (excessive daytime sleepiness not from inadequate sleep), F51.2 sleep-wake schedule disorder (circadian mismatch). Parasomnias — F51.3 sleepwalking, F51.4 sleep/night terrors (both arising in the first third of the night with limited recall), F51.5 nightmares (vivid, well-recalled, rapid orientation on waking).
ICD-10 routes organic sleep disorders to G47.- in the neurology chapter: G47.0 insomnia, G47.1 hypersomnia, G47.2 sleep-wake schedule, G47.4 narcolepsy, sleep apnoea, etc. F51 is reserved for the emotionally-driven, nonorganic presentations only. DSM-5 abandons this organic/nonorganic split entirely — its single Sleep–Wake Disorders chapter covers insomnia, hypersomnolence, narcolepsy, breathing-related, circadian, NREM/REM parasomnias and restless legs together, and explicitly allows a sleep diagnosis to coexist with a medical or psychiatric one rather than being subordinated to it.
Depression and anxiety (sleep change is a core symptom — code F51 only if it dominates), substance/medication effects and withdrawal, primary organic sleep disorders (apnoea, narcolepsy, restless legs), and shift-work / jet-lag circadian causes.
Paste your licensed Sleep–Wake Disorders criteria here.
Sexual dysfunction (nonorganic)F52▾
Ways in which a person cannot participate in a sexual relationship as they would wish, where the cause is judged not organic. The block walks the response cycle: desire (F52.0 loss of desire, F52.1 aversion / lack of enjoyment), arousal (F52.2 failure of genital response — erectile dysfunction in men, lubrication failure in women), orgasm (F52.3 orgasmic dysfunction, F52.4 premature ejaculation), and pain/spasm (F52.5 vaginismus, F52.6 dyspareunia — both the nonorganic forms). F52.7 covers excessive sexual drive.
DSM-5 keeps all sexual dysfunctions in one chapter and drops the ICD-10 organic/nonorganic distinction, instead requiring ≈ 6 months' duration and a frequency threshold and tagging each as lifelong/acquired and generalised/situational. It merged some ICD-10 entries — female desire and arousal became female sexual interest/arousal disorder; vaginismus and dyspareunia became genito-pelvic pain/penetration disorder. DSM places excessive sexual drive / "hypersexuality" outside this chapter (no formal diagnosis), whereas ICD-11 introduces compulsive sexual behaviour disorder under impulse-control.
Always exclude organic causes first (vascular, endocrine, neurological, pelvic pathology — these route to the relevant somatic chapter, e.g. N48.4 organic impotence, N94.1–.2 organic dyspareunia/vaginismus), plus medication effects (SSRIs, antihypertensives, antipsychotics), depression, and relationship factors.
Paste your licensed Sexual Dysfunctions criteria and specifiers here.
Puerperal disorders, NECF53▾
A residual, last-resort category for mental/behavioural disorders linked to the puerperium (onset within six weeks of delivery) that cannot be classified elsewhere — used only when information is insufficient, or when special clinical features make classification under the substantive disorder inappropriate. F53.0: mild (postnatal/postpartum depression NOS). F53.1: severe (puerperal psychosis NOS). The expectation is that a typical postnatal depression or psychosis is coded under its substantive category (mood/psychotic) first.
DSM-5 has no equivalent residual category. Instead it codes the underlying mood, psychotic, or other episode and appends a "with peripartum onset" specifier (onset in pregnancy or within four weeks postpartum) — note the four-week DSM window versus ICD-10's six weeks. This reflects a deliberate stance that postpartum illness is the same disorder with a timing modifier, not a distinct entity.
Puerperal psychosis is a psychiatric emergency (rapid onset, fluctuating course, infanticide/suicide risk) — urgent assessment and usually admission, ideally to a mother-and-baby unit. Screen for bipolar disorder, the strongest risk factor.
Paste your licensed peripartum-onset specifier criteria and local perinatal pathway here.
Psychological factors affecting physical conditionsF54▾
↗ F54 (no sub-codes — use an additional code for the physical disorder)
Records that psychological or behavioural influences played a major part in the aetiology of a physical disorder classified to another chapter. Any resulting mental disturbance is usually mild and prolonged (worry, emotional conflict, apprehension) and does not itself justify a separate diagnosis. ICD-10 lists worked examples pairing F54 with the somatic code: asthma (J45.-), dermatitis (L23–L25), gastric ulcer (K25.-), irritable bowel (K58.-), ulcerative colitis (K51.-), urticaria (L50.-). Always add the code for the physical condition.
DSM-5 keeps this as psychological factors affecting other medical conditions, sitting in the Somatic Symptom & Related Disorders chapter. The concept is closely aligned with ICD-10 F54 — a genuine medical condition is present, and psychological/behavioural factors adversely affect its course, treatment, or outcome.
Paste your licensed wording for psychological factors affecting other medical conditions here.
F99 — unspecified mental disorder ("mental disorder, not otherwise specified"). The one F-code that belongs to no block above: a genuine last resort for a mental disturbance that meets the general criteria for a mental disorder but fits none of F00–F98, or where information is too limited to place it. Use it only when no substantive category applies — and revisit the coding once more is known, since almost everything eventually finds a better home. (DSM-5 mirrors this with "unspecified mental disorder" 300.9 / F99; ICD-11 uses "mental disorder, unspecified" 6E8Z. Each block above also carries its own local residuals — e.g. F38/F39 for mood, F48 for other neurotic, F53 puerperal, F09 organic — which are preferred over F99 whenever the broad family is known.)
IIPsychopharmacology foundations
The mechanistic frame (Stahl's territory — orient and cite, don't copy) and the pharmacokinetics that drive dosing intervals, interactions, and monitoring.
Neurotransmitter systems & receptor actions
| System | Clinical relevance — what acting on it does |
|---|---|
| Dopamine (DA) | Mesolimbic overactivity → positive psychotic symptoms (D2 blockade treats them); nigrostriatal blockade → EPS; tuberoinfundibular blockade → hyperprolactinaemia; mesocortical hypofunction → negative/cognitive symptoms. |
| Serotonin (5-HT) | Mood, anxiety, sleep, appetite. 5-HT2A antagonism softens EPS and underlies the atypical profile; excess serotonergic tone → serotonin syndrome. |
| Noradrenaline (NE) | Arousal, attention, mood; SNRI/NRI action; α1 blockade → orthostasis; α2 antagonism (mirtazapine) → enhanced release. |
| GABA | Principal inhibitory transmitter; benzodiazepines/Z-drugs are positive allosteric modulators of GABA-A → sedation, anxiolysis, dependence. |
| Glutamate | Principal excitatory transmitter; NMDA-hypofunction model of psychosis; target of ketamine/esketamine and memantine. |
| Acetylcholine (ACh) | Muscarinic blockade → anticholinergic burden (dry mouth, constipation, urinary retention, cognitive impairment, delirium); central role in dementia. |
| Histamine (H1) | H1 blockade → sedation and weight gain (mirtazapine, olanzapine, quetiapine, many TCAs). |
The receptor-affinity fingerprints per drug, as a sourced master table, folded below — rank-order reliable, decimal-soft; verify before any clinical decision.
Binding affinities (Ki) & molecular targets — a sourced master reference, all classes▾
Read this first. A sourced master table of binding affinities and molecular targets, European/Romanian emphasis. Numbers are rank-order reliable, decimal-soft — Ki varies 3–10× across labs, radioligands, and species, and affinity (Ki) ≠ efficacy (agonist / antagonist / partial is stated separately). Several effective drugs (lithium, MAOIs, AChE-inhibitors, gabapentinoids) have no receptor Ki at all — they hit enzymes, ion channels, or auxiliary subunits (§7–8). 🇪🇺/🇷🇴 marks an agent characteristic of the European/Romanian market.
(1) Kd vs Ki — Richelson & Souder report Kd (post-mortem human brain); most others report Ki (cloned receptors). Comparable as rank-order, not identical. (2) Ki vs pKi — a documented mix-up (asenapine literature): a "Ki 8.9" that is really pKi 8.9 ≈ 1.3 nM, a ~7× error. Suspect pKi whenever a one-decimal "Ki" sits between ~5 and ~11. (3) Ki vs IC50/Kb — functional antagonists (orexin, some APs) are reported as Kb or IC50, convertible only under Cheng–Prusoff assumptions.
1 · Antidepressants transporters, multimodal, MAOIs▾
Transporters (SERT / NET / DAT, nM). Backbone: Tatsumi 1997 (human cloned transporters, single lab); escitalopram from Owens 2001.
| Drug | SERT | NET | DAT | Status |
|---|---|---|---|---|
| Paroxetine | 0.13 | ~40 | ~490 | ✓ verified SERT |
| Sertraline | ~0.29 | ~420 | 25 | ✓ verified DAT |
| Fluoxetine | ~0.81 | ~240 | ~3600 | ○ attributed |
| Citalopram | ~1.16 | ~4070 | ~28000 | ○ attributed |
| Escitalopram | ~1.1 | ≫1000 | ≫1000 | ○ attributed (Owens 2001) |
| Fluvoxamine | ~2.2 | ~1300 | ≫1000 | ○ attributed |
| Imipramine | 1.40 | ~37 | ~8500 | ✓ verified |
| Clomipramine | ~0.28 | ~38 | ~2200 | ○ attributed |
| Amitriptyline | ~4.3 | ~35 | ~3250 | ○ attributed |
| Nortriptyline | ~18 | ~4.4 | ~1140 | ○ attributed |
| Desipramine | ~163 | 0.83 | ~3190 | ✓ verified NET |
| Doxepin | ~68 | ~30 | ~12000 | ○ attributed |
| Maprotiline | ~5800 | ~11 | ~1000 | ○ attributed |
| Venlafaxine | 82 | 2480 | ≫9000 | ✓ verified |
| Duloxetine | 0.8 | 7.5 | ~240 | ✓ verified |
| Bupropion | ≫10000 | weak | ~520 | ○ attributed functional NDRI via metabolite + nAChR antag |
Receptor-target / multimodal antidepressants.
| Drug | Ki (nM) & action | Source | Status |
|---|---|---|---|
| Vortioxetine | SERT 1.6 (inhib); 5-HT1A 15 (agonist); 5-HT1B 33 (partial); 5-HT3A 3.7 (antag); 5-HT7 19 (antag); β1 46 | Bang-Andersen 2011 | ✓ verified |
| Vilazodone | SERT ~0.1 (inhib); 5-HT1A ~2.1 (partial agonist) | Hughes 2005 | ○ attributed |
| Agomelatine 🇪🇺 | MT1 0.06–0.2 & MT2 0.04–0.27 (agonist); 5-HT2C ~270 (antag) | Servier/Liu 2016 | ✓ verified |
| Tianeptine 🇪🇺🇷🇴 | MOR 383±183 (full agonist); DOR full agonist (weaker); KOR inactive; no monoamine/NMDA affinity | Gassaway 2014 | ✓ verified |
| Mirtazapine | H1 ~0.14; α2 ~20 (antag); 5-HT2A ~6–69; 5-HT2C ~8–39; 5-HT3 ~8 | de Boer 1996 | ○ attributed |
| Mianserin 🇪🇺 | H1 ~0.4; α2; 5-HT2A/2C (antag) | de Boer 1996 / PDSP | ○ attributed |
| Trazodone | 5-HT2A ~13–36 (antag); α1 ~25–42; SERT ~160–367; H1 ~220 | Cusack 1994 / PDSP | ○ attributed |
MAOIs — enzyme inhibitors, no receptor Ki. Moclobemide 🇪🇺🇷🇴 = reversible MAO-A (RIMA, low tyramine risk); tranylcypromine / phenelzine = irreversible MAO-A & MAO-B; selegiline = MAO-B (low dose) → MAO-A (patch/high dose).
2 · Antipsychotics D2/D3/5-HT2A/2C/7/H1/M1/α1▾
Backbone (older + first-wave atypicals): Richelson & Souder 2000 (human brain, Kd). Partial agonists & lurasidone from discovery papers.
| Drug | D2 | D3 | 5-HT2A | 5-HT2C | 5-HT7 | H1 | M1 | α1 | Action / note | Status |
|---|---|---|---|---|---|---|---|---|---|---|
| Haloperidol | ~0.7–1.4 | ~2–7 | ~25–120 | weak | — | ~440 | ≫1000 | ~6–19 | antagonist | ○ attributed |
| Chlorpromazine | ~1–6 | — | ~3–30 | ~16 | — | 0.18 | ~25 | ~0.3 | low-potency antagonist | ○ attributed |
| Sulpiride 🇪🇺 | ~7–15 | ~10–25 | ≫1000 | — | — | negl. | negl. | negl. | benzamide, poor BBB | ○ attributed |
| Amisulpride 🇪🇺 | 2.8 | 3.2 | ≫1000 | — | ~12–47 antag | negl. | negl. | negl. | presynaptic/limbic-selective; 5-HT7 | ✓ verified D2/D3 |
| Risperidone | ~3–4 | ~10 | ~0.2 | ~25 | ~3 | ~15–20 | ≫1000 | ~2–5 | 5-HT2A≫D2; no muscarinic | ✓ verified label |
| Paliperidone | ~2.8 | — | ~1.2 | ~48 | — | ~19 | ≫1000 | ~10 | 9-OH-risperidone | ○ attributed |
| Olanzapine | ~11–31 | — | ~1.5–4 | ~10–23 | — | 0.087 | ~1.9–26 | ~19 | most potent at H1 of set | ✓ verified H1 |
| Quetiapine | 770 | — | 31 | 3500 | — | 19 | 1400 | ~7–22 | low/transient D2; norquetiapine→NET/5-HT2C | ✓ verified |
| Clozapine | ~130–210 | ~9–21 (D4) | ~1.6–12 | ~5–17 | — | ~1–6 | 9 | ~1.6–7 | most potent at muscarinic; M4 partial agonist | ✓ verified M |
| Ziprasidone | ~3–7 | ~7 | ~0.4 | ~0.7 | ~9 | ~47 | ≫1000 | ~11 | 5-HT1A agonist | ✓ verified rank |
| Sertindole 🇪🇺 | ~0.45–2 | — | ~0.2–0.4 | ~0.9 | — | ~130 | ≫1000 | ~1.4 | QT prolongation | ○ attributed |
| Aripiprazole | ~0.34–3.4 | ~0.8 | ~3.4 antag | ~15 | — | ~28 | ≫1000 | ~26 | D2 partial; 5-HT1A partial; 5-HT2B inverse | ○ attributed |
| Brexpiprazole | ~0.3 | ~1.1 | ~0.47 | ~34 | ~3.7 | ~19 | — | ~0.17 (α1B) | D2 partial, lower intrinsic activity vs aripiprazole | ○ attributed |
| Cariprazine | 0.49 partial | 0.085 partial | ~18 | ~134 | — | ~23 | — | ~155 | D3-preferring (signature); 5-HT2B 0.6 antag; 5-HT1A 2.6 partial | ✓ verified |
| Lurasidone | 1.7 | ~16 | 2.0 | weak | 0.5 | negl. | negl. | α2C 10.8 | highest 5-HT7 affinity of APs; 5-HT1A 6.4 partial | ✓ verified |
3 · Anxiolytics & sedative-hypnotics GABA-A, orexin, melatonin▾
The "receptor Ki" frame only partly applies. Benzodiazepines are PAMs at the GABA-A BZ site (α+/γ2− interface, cryo-EM–confirmed) — per-drug BZ-site Ki are not standardised the way GPCR Ki are. Gabapentinoids bind an auxiliary channel subunit, not a GPCR. Only buspirone/hydroxyzine give a conventional receptor Ki.
| Drug / class | Target & action | Affinity (nM) | Status |
|---|---|---|---|
| Benzodiazepines (+ bromazepam, medazepam 🇪🇺) | PAM at GABA-A BZ site (α1=sedation/amnesia; α2/α3=anxiolysis/myorelaxation; α5=cognition) | No single Ki — α-subunit-resolved. Classic non-selective rank at the BZ site: clonazepam/flunitrazepam/lorazepam/triazolam ~1–3 > alprazolam/midazolam ~3–6 > diazepam ~10–15. Therapeutic BZDs are non-subtype-selective (hence sedation + anxiolysis together) | ○ attributed (subtype-dependent) |
| Buspirone | 5-HT1A partial agonist | ~10–20 (5-HT1A); D2 ~98 weak | ○ attributed |
| Hydroxyzine | H1 antagonist (anxiolytic) | H1 ~2 | ○ attributed |
| Z-drugs (zolpidem; zopiclone 🇪🇺, zaleplon) | GABA-A PAM, α1-preferring (zolpidem) | BZ-site; zolpidem α1-selective | ○ attributed (mechanism solid) |
| Pregabalin / gabapentin | α2δ-1 subunit of VGCC (↓ glutamate/NE release) | high-affinity at α2δ (not a GPCR Ki) | ○ attributed |
| Etifoxine 🇪🇺 | GABA-A direct modulation + TSPO | profile only | ○ attributed |
Orexin antagonists (hypnotics) — functional Kb/Ki, nM.
| Drug | OX1 | OX2 | Profile | Status |
|---|---|---|---|---|
| Suvorexant | ~0.7 | ~1.0 | dual, insurmountable | ✓ verified |
| Lemborexant | ~13 | ~0.4 | OX2-preferential, short residence | ✓ verified |
| Daridorexant 🇪🇺 | ~0.5 | ~0.8 | dual, equipotent; only DORA approved in EU | ✓ verified |
Melatonin-receptor hypnotics. Ramelteon — MT1 14 pM / MT2 112 pM (agonist; picomolar, MT3-sparing, highly selective; ✓ verified). Tasimelteon — MT1 ~0.3 nM / MT2 ~0.1–0.2 nM (slightly MT2-preferring; non-24h disorder; ○ attributed). Agomelatine is listed under antidepressants above.
4 · ADHD agents transporters & α2A▾
Stimulant transporter selectivity: Han & Gu 2006. Methylphenidate blocks DAT/NET but is ~1000× weaker at SERT; amphetamine/methamphetamine are most potent at NET and act as releasers (transporter substrates), not just blockers.
| Drug | Target & action | Affinity (nM) | Status |
|---|---|---|---|
| Methylphenidate | DAT/NET reuptake blocker | DAT ~34–200; NET ~339; SERT ≫1000 | ○ attributed (rank ✓ verified) |
| Amphetamine / lisdex. | DA/NE releaser + reuptake | most potent at NET; DAT 5–9× less; SERT 200–500× less | ○ attributed (rank ✓ verified) |
| Atomoxetine | Selective NET inhibitor | NET 5; 5-HT 77; DAT 1451 | ✓ verified |
| Guanfacine | α2A-adrenergic agonist (postsynaptic, PFC) | α2A-preferring (Ki not standardised) | ○ attributed (mechanism solid) |
| Clonidine | α2-adrenergic agonist (α2A>2B/2C; presynaptic LC) | high α2 affinity | ○ attributed |
5 · Substance-use / addiction agents opioid, alcohol, nicotine▾
Opioid use disorder — µ-opioid receptor (MOR), nM. Source: Volpe 2011.
| Drug | MOR & action | Affinity | Status |
|---|---|---|---|
| Buprenorphine | partial agonist (MOR); KOR antagonist | MOR very high (~0.2 nM); slow dissociation | ○ attributed (rank ✓ verified) |
| Methadone | full agonist (MOR) | MOR ~3–4 nM | ○ attributed |
| Naltrexone | antagonist (MOR≈KOR) | MOR ~0.5–1 nM | ○ attributed |
| Naloxone | antagonist | MOR ~1–2 nM | ○ attributed |
Alcohol use disorder. Naltrexone — MOR antagonist (↓ reward). Nalmefene 🇪🇺 — MOR antagonist + KOR partial agonist (EU: as-needed reduction). Acamprosate — NMDA/glutamate + GABA modulation (mechanism imprecise). Disulfiram — ALDH inhibitor (enzyme, aversive; not a receptor).
Nicotine. Varenicline — α4β2 nAChR partial agonist (>500× selective vs α3β4; 5-HT3 Ki 350 nM; ✓ verified). Bupropion — nAChR antagonist + weak NDRI. Cytisine 🇪🇺 — α4β2 partial agonist (Tabex, Eastern Europe).
6 · Dementia / cognition agents AChE-I, memantine, anti-amyloid▾
| Drug | Target & action | Affinity | Status |
|---|---|---|---|
| Donepezil | Acetylcholinesterase inhibitor — enzyme | AChE IC50 ~6 nM | ○ attributed |
| Rivastigmine | AChE + butyrylcholinesterase inhibitor | — | ○ attributed |
| Galantamine | AChE inhibitor + allosteric nAChR potentiator | — | ○ attributed |
| Memantine | Low-affinity, uncompetitive NMDA open-channel blocker; fast off-rate (vs MK-801) | NMDA Ki ~0.5–1 µM | ○ attributed |
| Anti-amyloid mAbs (lecanemab, donanemab) | Aβ-directed monoclonal antibodies (disease-modifying); not receptor ligands | — | ○ attributed |
7 · Mood stabilisers intracellular / ion-channel — no receptor Ki▾
The clearest illustration of why a Ki table can't capture psychopharmacology: none of the canonical mood stabilisers acts at a neurotransmitter receptor.
| Drug | Target(s) | Status |
|---|---|---|
| Lithium | Inhibits inositol monophosphatase (IMPase, low-mM) → inositol depletion; inhibits GSK-3α/β (competes with Mg²⁺); also BPNT, β-arrestin2 | ✓ verified (mechanism) |
| Valproate | Voltage-gated Na⁺ channel; ↑GABA turnover; HDAC inhibition; inositol-pathway effects (GSK-3 inhibition contested — not in therapeutic range) | ○ attributed |
| Lamotrigine | Use-dependent voltage-gated Na⁺ channel blocker → ↓ glutamate release | ○ attributed |
| Carbamazepine / oxcarbazepine | Use-dependent Na⁺ channel blocker; stimulates IMPase (opposite of lithium) | ○ attributed |
8 · Quick “no-Ki” index the common confusions▾
MAOIs (moclobemide, tranylcypromine, phenelzine, selegiline) → MAO enzyme · Lithium → IMPase / GSK-3 · Valproate / lamotrigine / carbamazepine → Na⁺ channels (± HDAC, inositol) · AChE-inhibitors (donepezil, rivastigmine, galantamine) → cholinesterase enzyme · Disulfiram → ALDH enzyme · Gabapentin / pregabalin → α2δ Ca²⁺-channel subunit · Acamprosate → glutamatergic modulation (imprecise) · Anti-amyloid mAbs → Aβ protein.
References primary sources & databases▾
PK essentials & CYP450
Steady state is reached in roughly 5 half-lives of constant dosing (same for a dose change or washout). Short-t½ drugs (venlafaxine, paroxetine) → sharper discontinuation; long-t½ (fluoxetine + active metabolite) → self-taper. Plasma monitoring is routine for lithium, clozapine, valproate, carbamazepine, and useful where adherence/toxicity/interactions are in question.
An inhibitor raises a co-prescribed substrate's level (toxicity risk); an inducer lowers it (loss of effect). Key players: CYP2D6 (fluoxetine/paroxetine/bupropion inhibit), CYP3A4 (carbamazepine strongly induces), CYP1A2 (tobacco smoke induces → stopping smoking raises clozapine levels). Use the Flockhart table (Part V).
One place for CYP/PK interactions and within-class differences (the former Part V section and the side-effects/CYP dossier, brought together here).
↗ Flockhart CYP450 table (Indiana University) · ↗ CredibleMeds — QT/TdP lists (free registration)
CYP inhibition/induction: check any new combination on Flockhart — fluoxetine/paroxetine/bupropion inhibit CYP2D6; carbamazepine strongly induces CYP3A4; smoking induces CYP1A2 (clozapine/olanzapine levels fall on cessation). Serotonergic stacking: highest risk with MAOIs + SSRIs/SNRIs/TCAs and hidden serotonergics → serotonin syndrome. QT stacking: avoid combining QT-prolongers; correct K⁺/Mg²⁺. Lithium: NSAIDs, ACE-i/ARB, thiazides, dehydration raise levels toward toxicity.
Add the specific interaction pairs most relevant to your caseload.
Side effects, half-lives & CYP interactions — within-class differences, in depth▾
The premise. A drug class is not a monolith — agents share a mechanism but diverge in receptor side-affinities, half-life, and CYP450 metabolism, and therefore in tolerability and interaction risk. Frequencies follow the EMA convention; PK and enzyme assignments are representative and vary with formulation, age, organ function, and CYP genotype (PM/IM/EM/UM). The individual current SmPC (Rezumatul Caracteristicilor Produsului) and a live interaction checker are authoritative.
Very common (foarte frecvente) ≥ 1/10 · Common (frecvente) 1/100–1/10 · Uncommon 1/1,000–1/100 · Rare 1/10,000–1/1,000 · Very rare < 1/10,000 · Not known (post-marketing, cannot be estimated).
Substrate = broken down by that enzyme; inhibiting the enzyme raises the substrate (toxicity), inducing it lowers the substrate (loss of effect). Inhibition is fast (days); induction is slow (1–3 weeks) and so is de-induction. Inhibitor / inducer = the drug changes an enzyme's activity, affecting other co-prescribed substrates.
CYP450 — the major psychiatric enzymes substrates · inhibitors · inducers▾
| Enzyme | Key psychiatric substrates | Inhibitors (↑ substrate) | Inducers (↓ substrate) |
|---|---|---|---|
| CYP1A2 | Clozapine, olanzapine, duloxetine, agomelatine, mirtazapine, TCAs, caffeine, theophylline | Fluvoxamine (potent), ciprofloxacin, caffeine (competitive), OCPs | Tobacco/cannabis smoke (PAHs, not nicotine), carbamazepine, chargrilled food |
| CYP2D6 | Risperidone, aripiprazole, haloperidol, TCAs, venlafaxine, atomoxetine, codeine/tramadol (activation), tamoxifen (activation), metoprolol | Paroxetine, fluoxetine, bupropion (potent); duloxetine, sertraline (mod) | Not inducible; activity is genetic (PM/UM phenotypes) |
| CYP2C19 | Citalopram, escitalopram, sertraline, diazepam, clomipramine, amitriptyline | Fluvoxamine, fluoxetine, esomeprazole | Carbamazepine, rifampicin, St John's Wort |
| CYP3A4 | Quetiapine, ziprasidone, lurasidone, pimozide, carbamazepine, midazolam/alprazolam, pregabalin (minor) | Ketoconazole/itraconazole, clarithromycin, ritonavir, grapefruit, nefazodone | Carbamazepine, phenytoin, rifampicin, St John's Wort |
| UGT (glucuronidation) | Lorazepam, oxazepam, temazepam, lamotrigine | Valproate (inhibits lamotrigine UGT) | Smoking, carbamazepine, OCPs (lower lamotrigine) |
Caffeine up front: caffeine is both a CYP1A2 substrate and a competitive CYP1A2 inhibitor. Heavy intake can raise clozapine/olanzapine levels; conversely those drugs slow caffeine clearance, so patients feel more "wired" on the same coffee. The bigger 1A2 lever is smoking — see its dedicated fold.
1 · Antidepressants SSRI · SNRI · TCA · others▾
Very common: nausea, headache, dry mouth, somnolence/insomnia, sexual dysfunction (often persistent, under-elicited). Common: GI change, hyperhidrosis, dizziness, tremor, agitation/anxiety, appetite/weight change, fatigue, blurred vision, yawning. Uncommon: bruising/bleeding, mydriasis, tachycardia, urinary disturbance. Rare: hyponatraemia/SIADH, serotonin syndrome, GI haemorrhage, hepatic dysfunction, seizures. Very rare/not known: QT prolongation, akathisia, movement disorders, hypomanic switch, angle-closure glaucoma.
Paroxetine's muscarinic affinity + short half-life make it the side-effect outlier; fluvoxamine, fluoxetine, paroxetine are the interaction outliers (potent CYP inhibitors). Sertraline/citalopram/escitalopram are comparatively "clean" — a major reason they're preferred in polypharmacy.
| Agent | t½ | Metabolism (substrate) | CYP inhibition caused | Distinguishing signal |
|---|---|---|---|---|
| Sertraline | ~26 h | 2C19, 2D6, 3A4 | Weak–mod 2D6 (dose-dep); mild | Most diarrhoea/GI; balanced; polypharmacy-friendly |
| Escitalopram | ~27–30 h | 2C19, 2D6, 3A4 | Minimal | Cleanest; dose-dependent QT; 2C19 PMs lower dose |
| Citalopram | ~35 h | 2C19, 2D6, 3A4 | Minimal–weak | Highest QT of class; 2C19 inhibitors (omeprazole) ↑ levels → QT |
| Fluoxetine | 4–6 days (norfluox. wks) | 2D6, 2C9 | Potent 2D6, mod 2C19/3A4 | Most activating; lowest weight gain; negligible discontinuation; long inhibitory tail |
| Paroxetine | ~21 h | 2D6 | Potent 2D6 | Most anticholinergic/weight/sexual; worst discontinuation; avoid in elderly (Beers), pregnancy |
| Fluvoxamine | ~15 h | 2D6, 1A2 | Potent 1A2 + 2C19; mod 3A4 | Most nausea; highest interaction burden — ↑ clozapine up to ~2×, theophylline, caffeine |
Concrete SSRI interactions: fluoxetine/paroxetine + tamoxifen → ↓ endoxifen → reduced efficacy (prefer escitalopram/venlafaxine). Fluoxetine/paroxetine + metoprolol/TCAs/codeine-tramadol → raise levels (or reduce analgesia by blocking activation). Fluvoxamine + clozapine/theophylline/tizanidine → toxic via 1A2. Any SSRI + NSAID/anticoagulant/antiplatelet → additive bleeding.
SNRIs
Very common: nausea, dry mouth, headache, hyperhidrosis, somnolence, dizziness. Common: hypertension/BP rise, constipation, insomnia, sexual dysfunction, ↓ appetite, tremor, palpitations, mydriasis, asthenia. Uncommon–rare: tachycardia, syncope, urinary retention, bruxism, hyponatraemia, serotonin syndrome, hepatotoxicity (duloxetine), mania switch.
| Agent | t½ | Metabolism | Inhibition | Distinguishing signal |
|---|---|---|---|---|
| Venlafaxine | ~5 h (+ODV ~11 h) | 2D6→active ODV; 3A4 | Minimal | Dose-dependent hypertension (>150 mg); worst discontinuation; highest overdose lethality of modern ADs |
| Desvenlafaxine | ~11 h | Mainly UGT | Minimal | Fewer CYP interactions; similar BP signal |
| Duloxetine | ~12 h | 1A2 + 2D6 | Moderate 2D6 | More start-up nausea; hepatotoxicity (avoid hepatic impairment/alcohol); 1A2 inhibitors + smoking shift levels |
| Milnacipran | ~8 h | Mainly renal/UGT | Minimal | More noradrenergic; dysuria; few interactions |
Tricyclics (TCAs)
Very common: anticholinergic (dry mouth, constipation, blurred vision), sedation, weight gain, orthostatic hypotension, dizziness. Common–uncommon: urinary retention, tachycardia, sweating, tremor, confusion (elderly), sexual dysfunction, conduction delay. Rare: cardiotoxic/lethal in overdose (narrow index), seizures, agranulocytosis, cholestatic jaundice, mania switch.
Metabolism: substrates of CYP2D6 (and 2C19/1A2/3A4) — dangerous victims of interaction. A potent 2D6 inhibitor (fluoxetine, paroxetine, bupropion) can push TCA levels toward cardiotoxic/seizure range — check levels when combining. Tertiary amines also use 1A2/2C19 (smoking and 2C19 status shift them).
| Agent | Type | Distinguishing signal |
|---|---|---|
| Amitriptyline | Tertiary | Most sedating/anticholinergic; low-dose for pain/sleep |
| Clomipramine | Tertiary | Most serotonergic (OCD); highest seizure risk |
| Imipramine | Tertiary | Marked orthostatic hypotension |
| Nortriptyline | Secondary | Best tolerated; least anticholinergic; TDM available |
| Doxepin | Tertiary | Strong antihistamine; very-low-dose for insomnia |
Other antidepressants
| Agent | t½ | Metabolism / interaction | Distinguishing profile |
|---|---|---|---|
| Mirtazapine | ~20–40 h | 1A2/2D6/3A4 substrate; not a significant inhibitor | Sedation, appetite/weight gain; few sexual/GI effects; sedation paradoxically less at higher dose; rare agranulocytosis |
| Bupropion | ~20 h | 2B6 substrate; potent 2D6 inhibitor | Activating, weight-neutral, minimal sexual dysfunction; dose-dependent seizures (CI seizure/eating disorders, alcohol/benzo withdrawal); raises 2D6 substrates incl. tamoxifen risk |
| Trazodone | ~7 h | 3A4 substrate | Sedating (low-dose for sleep), orthostasis; priapism (rare); 3A4 inhibitors ↑ levels |
| Vortioxetine | ~66 h | 2D6 substrate | Mainly dose-related nausea; low sexual dysfunction; 2D6 inhibitors/PM ↑ levels |
| Agomelatine | ~1–2 h | 1A2 substrate — fluvoxamine contraindicated | Sleep benefit, weight/sexual-neutral; hepatotoxicity → mandatory LFT monitoring; CI hepatic impairment |
| MAOIs (tranylcypromine; moclobemide) | short | — | Hypertensive crisis with tyramine; serotonin syndrome with serotonergic co-Rx (washout — note fluoxetine's long tail) |
2 · Antipsychotics SGA & FGA — metabolic/EPS/enzyme▾
Very common: weight gain, sedation/somnolence, metabolic changes (agent-dependent). Common: EPS (akathisia, parkinsonism, tremor), hyperprolactinaemia, orthostatic hypotension, dizziness, constipation, dry mouth, QTc prolongation. Uncommon–rare: tardive dyskinesia, seizures, NMS, severe hyperglycaemia/DKA, VTE, QT arrhythmia. Very rare/not known: agranulocytosis & myocarditis (clozapine), severe cutaneous reactions, priapism.
The metabolic-vs-EPS/prolactin trade-off drives drug choice; the metabolising enzyme drives interaction and smoking sensitivity. Crucially, clozapine and olanzapine are CYP1A2 substrates → strongly affected by smoking and caffeine, while risperidone/aripiprazole (2D6) and quetiapine/lurasidone/ziprasidone (3A4) are not.
| Agent | t½ | Weight/metab | EPS | Prolactin | QTc | Metabolism | Smoke/caffeine? |
|---|---|---|---|---|---|---|---|
| Olanzapine | ~33 h (≈52 elderly) | Very high | Low | Low–mod | Low | 1A2 + UGT | Yes — smokers need ↑ dose; cessation ↑ levels |
| Clozapine | ~12 h (4–66) | Very high | Very low | Low | Mod | 1A2 major, 3A4/2D6 minor | Yes, critically — TDM essential |
| Quetiapine | ~7 h (norquet. 9–12) | Mod–high | Very low | Low | Mod | 3A4 | No (3A4 modulators matter) |
| Risperidone | ~20 h oral | Moderate | Dose-dep ↑ | High | Mod | 2D6→paliperidone | No (2D6 inhibitors ↑) |
| Paliperidone | ~23 h oral | Moderate | Moderate | High | Mod | Mostly renal | No |
| Aripiprazole | ~75 h (metab ~94) | Low | Akathisia | Low | Low | 2D6 + 3A4 | No; halve dose with 2D6/strong-3A4 inhibitors |
| Cariprazine | ~1 wk effective | Low | Akathisia | Low | Low | 3A4 | No; very long t½ → delayed onset/offset |
| Amisulpride | ~12 h | Low–mod | Dose-dep | Very high | Dose-dep ↑ | Mostly renal | No |
| Ziprasidone | ~7 h | Low | Low | Low | High | 3A4 + aldehyde oxidase | No; take with food (≥500 kcal) |
| Lurasidone | ~18–40 h | Low | Akathisia | Low–mod | Low | 3A4 (sensitive) | No; avoid strong 3A4 inhibitors/inducers; food (≥350 kcal) |
Concrete interactions: quetiapine/lurasidone/ziprasidone + strong 3A4 inhibitor (clarithromycin, ketoconazole, ritonavir, grapefruit) → ↑ levels (sedation, QT); + carbamazepine → loss of effect (lurasidone: strong 3A4 modulators contraindicated). Risperidone/aripiprazole + paroxetine/fluoxetine/bupropion → ↑ levels (aripiprazole label: halve dose). Olanzapine/clozapine + fluvoxamine/ciprofloxacin → ↑ levels; + smoking → ↓ levels.
First-generation
Very common/common: high-potency → EPS (dystonia, parkinsonism, akathisia) + hyperprolactinaemia; low-potency → sedation, anticholinergic, hypotension. Uncommon–rare: tardive dyskinesia (cumulative), QT prolongation, seizures, photosensitivity (chlorpromazine), cholestatic jaundice. Rare/very rare: NMS, agranulocytosis, sudden cardiac death.
| Agent | Potency | t½ | Metabolism | Distinguishing signal |
|---|---|---|---|---|
| Haloperidol | High | ~14–21 h | 2D6, 3A4 (+1A2) | Marked EPS; QT (esp. IV); smoking and 2D6/3A4 modulators shift levels |
| Flupentixol / Zuclopenthixol | Mid–high | ~20–35 h oral | 2D6 | EPS-prone; depot available |
| Chlorpromazine | Low | ~30 h | 2D6, 1A2 | Most sedating/hypotensive/anticholinergic; photosensitivity/pigmentation |
| Levomepromazine | Low | ~15–30 h | — | Very sedating; palliative care |
Cross-class: ↑ mortality / cerebrovascular events with antipsychotics in dementia-related behavioural symptoms (EU-wide, all agents).
3 · Anxiolytics & hypnotics benzodiazepines · Z-drugs · others▾
Very common/common: sedation, drowsiness, reduced alertness, ataxia, anterograde amnesia, psychomotor/cognitive impairment, muscle weakness. Uncommon: confusion (elderly), depressed mood, diplopia, dysarthria, ↓ libido. Rare: paradoxical reactions (agitation, disinhibition, aggression), respiratory depression (potentiated by opioids/alcohol). Not known: falls/fractures (elderly), dependence and tolerance.
Clinical differences are pharmacokinetic. The metabolic split matters for safety: most are CYP3A4 substrates, but lorazepam, oxazepam, temazepam are cleared by glucuronidation (UGT) only — no oxidative metabolism, making them the safe choice in hepatic impairment, the elderly, and heavy CYP polypharmacy.
| Agent | Onset | t½ (± active metab) | Potency | Metabolism | Distinguishing signal |
|---|---|---|---|---|---|
| Alprazolam | Fast | Short (~11–12 h) | High | 3A4 | Most reinforcing/misused; interdose rebound; hardest taper; 3A4 inhibitors ↑ markedly |
| Lorazepam | Intermediate | ~12 h | High | UGT only | No CYP → preferred in hepatic impairment/elderly/interactions |
| Oxazepam | Slow | Intermediate | Low | UGT only | Slow onset, low misuse; elderly-friendly |
| Bromazepam 🇪🇺 | Intermediate | Intermediate | Mid | CYP (oxidative) | Common EU anxiolytic |
| Clonazepam | Intermediate | Long (~18–50 h) | High | 3A4 | All-day cover; smoother withdrawal than alprazolam; accumulation |
| Diazepam | Fast (lipophilic) | Very long (active metab, days) | Low | 2C19 + 3A4 | Rapid onset; long self-tapering tail → used to taper off shorter agents; 2C19 status/inhibitors prolong |
Z-drugs & others
| Agent | t½ | Metabolism | Distinguishing signal |
|---|---|---|---|
| Zolpidem | ~2.5 h | 3A4 | Complex sleep behaviours (sleep-driving/eating — discontinue); 3A4 inhibitors ↑, inducers ↓ |
| Zopiclone 🇪🇺 | ~5 h | 3A4, 2C8 | Most residual drowsiness of Z-drugs; metallic taste |
| Zaleplon | ~1 h | Aldehyde oxidase, 3A4 | Least hangover (shortest t½) |
| Buspirone | ~2–3 h | 3A4 (sensitive) | Non-sedating, no dependence, delayed onset; grapefruit/3A4 inhibitors ↑ markedly; avoid with MAOIs |
| Pregabalin (GAD) | ~6 h | Renal (negligible CYP) | Dizziness, somnolence, weight gain, oedema, euphoria; misuse/dependence; additive CNS/opioid depression |
| Hydroxyzine | ~20 h | — | Sedation, dry mouth; dose-dependent QT |
4 · Mood stabilisers lithium · valproate · lamotrigine · carbamazepine▾
Not a shared-mechanism class — differences define drug choice. Carbamazepine is the dominant interaction hazard (potent broad inducer + autoinducer); lamotrigine is the notable victim (valproate doubles it).
| Agent | t½ | Weight | Teratogenicity | Signature serious risk | Metabolism / enzyme effect | Monitoring |
|---|---|---|---|---|---|---|
| Lithium | ~18–24 h (↑ elderly/renal) | ↑ | Moderate (Ebstein's) | Narrow index — toxicity; CKD; thyroid/parathyroid | Renal (no CYP). Levels ↑ by NSAIDs, ACEi/ARB, thiazides, dehydration, low Na⁺ | Levels, eGFR, TSH, Ca²⁺ |
| Valproate | ~9–16 h | ↑↑ | Highest | Hepatotoxicity, pancreatitis, hyperammonaemia, thrombocytopenia | UGT + CYP; inhibits UGT → doubles lamotrigine | LFTs, FBC, ammonia |
| Lamotrigine | ~25–33 h alone; ~60–70 with valproate; ~13–15 with CBZ | Neutral | Lower | SJS/TEN (titration-dependent) | UGT; halved by carbamazepine/OCPs, doubled by valproate | Clinical (rash); slow titration |
| Carbamazepine | ~35 h single → ~10–20 chronic (autoinduction ~3–4 wk) | Neutral/↑ | NTDs | SJS/TEN (HLA-B*15:02), aplastic anaemia | Potent inducer of 3A4, 1A2, 2C19 + UGT; autoinducer | FBC, LFTs, Na⁺, levels |
Lithium — maintenance ~0.6–0.8 mmol/L; toxicity >1.2–1.5. No CYP; interaction hazards are pharmacokinetic via the kidney (NSAIDs, ACEi/ARB, thiazides, dehydration ↑ lithium; caffeine's mild diuresis can lower it, so cutting caffeine can raise levels). Valproate — inhibits glucuronidation → doubles lamotrigine (halve lamotrigine titration); most teratogenic psychotropic, contraindicated without a pregnancy-prevention programme (ANM/EU). Lamotrigine — valproate doubles it; carbamazepine, phenytoin, and oestrogen-containing contraceptives halve it (levels drop in the pill-free week); metabolically clean → favoured for bipolar depression. Carbamazepine — the biggest interaction liability here: lowers efficacy of hormonal contraceptives, many antipsychotics (quetiapine, aripiprazole, lurasidone), lamotrigine, DOACs, methadone; HLA-B*15:02 screen in at-risk ancestries; teratogenic (NTDs).
5 · ADHD medications stimulants & non-stimulants▾
Very common/common: ↓ appetite, insomnia, headache, weight loss, ↑ HR/BP, dry mouth, abdominal pain/nausea, irritability/anxiety/mood lability, tremor. Uncommon: palpitations, tics, growth-velocity reduction (children), bruxism. Rare/very rare: psychotic/manic symptoms, seizures, priapism (amphetamines), peripheral vasculopathy/Raynaud's. Not known: CV events in structural cardiac disease; misuse/diversion.
Methylphenidate blocks DA/NA reuptake; amphetamines also release them. Network meta-analysis: amphetamines more efficacious but less tolerated; methylphenidate better tolerated (EU/NICE: methylphenidate first-line in children). Metabolism is non-CYP, so CYP interactions are minimal — but additive sympathomimetic/CNS stimulation with caffeine is real.
| Agent | Class | t½ / clinical duration | Metabolism | Distinguishing signal |
|---|---|---|---|---|
| Methylphenidate (IR/OROS) | MPH | t½ ~2–3 h; IR ~3–4 h, OROS/XR ~8–12 h | Carboxylesterase (CES1A1) — non-CYP | Better tolerated; rebound as IR wears off (OROS smooths); more headache/nasopharyngitis |
| Dexmethylphenidate | MPH | t½ ~2–4.5 h; XR ~8–12 h | CES1A1 | Active enantiomer; lower dose |
| Lisdexamfetamine | Amphetamine prodrug | prodrug t½ <1 h; dexamfet. ~10–12 h; effect ~12–13 h | RBC hydrolysis to dexamfetamine | Smooth, lower misuse (prodrug); more appetite suppression/weight loss/insomnia |
| Dexamfetamine | Amphetamine | t½ ~10–12 h; IR effect ~4–6 h | CYP2D6 (partial) + deamination | Short-acting; greater efficacy; higher misuse; 2D6 status modulates; urinary pH alters clearance |
Non-stimulants
| Agent | t½ | Metabolism | Distinguishing signal |
|---|---|---|---|
| Atomoxetine | ~5 h (EM) → ~21–24 h in 2D6 PMs | 2D6 | ↓ appetite, nausea, dry mouth, insomnia, ↑ HR/BP, ED. Rare: hepatotoxicity, suicidal ideation (youth). 2D6 PMs / paroxetine/fluoxetine → much higher exposure; non-controlled |
| Guanfacine XR | ~17–18 h | 3A4 | Somnolence, hypotension, bradycardia; do not stop abruptly (rebound hypertension); 3A4 inhibitors ↑, inducers (carbamazepine) ↓ |
CYP1A2, smoking & caffeine the most clinically missed interaction▾
This deserves its own fold because it is common, large, and frequently overlooked on wards.
- Tobacco and cannabis smoke (the polycyclic aromatic hydrocarbons, not nicotine) are potent CYP1A2 inducers. Smokers metabolise clozapine and olanzapine much faster and need higher doses.
- Stopping smoking (planned quit, or forced abstinence on admission) removes the induction over 1–2 weeks → clozapine/olanzapine levels can rise sharply into the toxic range (sedation, seizures, hypotension). Reduce dose proactively and use TDM. Nicotine replacement does NOT induce CYP1A2 — only the smoke does, so NRT does not substitute for the lost induction.
- Caffeine competitively inhibits CYP1A2 and is itself a substrate: heavy intake can raise clozapine/olanzapine levels; a sudden change in coffee consumption shifts them.
- Fluvoxamine and ciprofloxacin are potent CYP1A2 inhibitors — combining either with clozapine can roughly double clozapine levels.
| Change | Effect on CYP1A2 | Effect on clozapine/olanzapine level |
|---|---|---|
| Start / smoke heavily | Induced | ↓ (may lose effect) |
| Stop smoking (incl. admission) | De-induced over 1–2 wks | ↑↑ (toxicity risk — reduce dose, TDM) |
| Start fluvoxamine or ciprofloxacin | Inhibited | ↑↑ |
| Marked ↑ caffeine | Inhibited (competitive) | ↑ |
| Nicotine patch/gum (no smoke) | No change | No change |
Cross-class quick-reference signature reactions & key CYP pairs▾
Signature serious reactions — strongest within-class offenders.
| Reaction | Strongest offenders |
|---|---|
| Serotonin syndrome | SSRIs/SNRIs/MAOIs + serotonergic combos (tramadol, triptans, linezolid) |
| NMS | High-potency FGAs (haloperidol) > SGAs |
| QT prolongation | Citalopram > escitalopram; ziprasidone, amisulpride, haloperidol, hydroxyzine, TCAs |
| Agranulocytosis | Clozapine (registry), carbamazepine, mirtazapine (rare) |
| SJS/TEN/DRESS | Carbamazepine (HLA-B*15:02), lamotrigine (rapid titration/valproate) |
| Hepatotoxicity | Valproate, agomelatine, atomoxetine, duloxetine |
| Hyponatraemia/SIADH | SSRIs/SNRIs (elderly), carbamazepine |
| Metabolic / weight gain | Olanzapine > clozapine > quetiapine; mirtazapine, paroxetine; valproate, lithium |
| Dependence / withdrawal | Alprazolam > other benzodiazepines; Z-drugs; pregabalin; (discontinuation: paroxetine, venlafaxine) |
| Teratogenicity | Valproate (highest) > carbamazepine, lithium > lamotrigine |
| Major CYP interaction source | Fluvoxamine (1A2/2C19), fluoxetine/paroxetine/bupropion (2D6), carbamazepine (broad inducer), smoking (1A2) |
Fluvoxamine + clozapine/theophylline → toxicity (1A2). Fluoxetine/paroxetine/bupropion + tamoxifen → loss of efficacy (2D6). Fluoxetine/paroxetine + TCA or metoprolol → ↑ substrate (2D6). Carbamazepine + (contraceptive / quetiapine / lamotrigine / DOAC) → loss of effect (broad induction). Valproate + lamotrigine → ↑ lamotrigine, rash risk (UGT inhibition). Stop smoking on a clozapine/olanzapine patient → rising levels (1A2 de-induction). Strong 3A4 inhibitor (clarithromycin, grapefruit, ritonavir) + quetiapine/lurasidone/alprazolam/buspirone → ↑ levels. Lithium + (NSAID / ACEi / thiazide / dehydration) → lithium toxicity (renal).
Romania-specific practice notes SmPC · ANM · controlled drugs▾
The Romanian SmPC (Rezumatul Caracteristicilor Produsului) is the EMA-harmonised label; the frequency descriptors, PK, and interaction warnings above map directly — confirm the current ANM entry for the specific brand/product. The valproate pregnancy-prevention programme is in force (ANM/EU) for women and girls of childbearing potential. Controlled substances (stimulants, most benzodiazepines) follow Romanian narcotic/psychotropic prescribing regulations (special forms and dispensing rules). Report suspected adverse reactions to ANM / EudraVigilance.
Pharmacodynamic interactions additive-effect traps — distinct from CYP/PK▾
Everything above is pharmacokinetic (one drug changes another’s level via CYP/UGT). Pharmacodynamic interactions are additive effects at normal levels — the commoner real-world trap, and invisible to a checker that only flags CYP.
Additive serotonergic → serotonin syndrome: stacking SSRIs/SNRIs/TCAs/MAOIs with tramadol, pethidine, linezolid, methylene blue, triptans, or St John’s wort (cross-reference SS vs NMS and MAOI). Additive QTc → torsades: two or more QT-prolonging drugs (citalopram, haloperidol, methadone, some antiemetics/antibiotics) plus hypokalaemia/hypomagnesaemia (cross-reference QTc). Additive sedation / anticholinergic / CNS depression: benzodiazepines + opioids + alcohol (respiratory depression); and cumulative antimuscarinic load (TCAs, low-potency antipsychotics, antihistamines, oxybutynin) → confusion and falls in the elderly (cross-reference anticholinergic toxicity).
Add your serotonergic / QT / sedation-burden checklist for polypharmacy review.
Receptor mechanisms across disorders
A synthesis dossier — treatment-back-to-hypothesis — kept folded; it sits with the pharmacology foundations it draws on.
Receptor mechanisms across disorders — a synthesis, treatment-back to hypothesis▾
Read this first. Most entries describe the pharmacology of treatments (well-characterised) and the pathophysiological hypothesis inferred backwards from them (often weak). "Receptor X is implicated in disorder Y" usually means "a drug acting on X helps" — not the same as X being causal. The actual etiology of nearly every disorder here remains unknown.
Cross-cutting primer — pre/post-synaptic logic the autoreceptor stories▾
Half the "delayed onset" and "paradoxical" stories in psychiatry are autoreceptor stories. The recurring motifs worth holding in your head:
- 5-HT1A (Gi-coupled). Somatodendritic autoreceptors on raphe neurons (presynaptic, inhibit firing) vs postsynaptic receptors (hippocampus, PFC; mediate the anxiolytic/antidepressant effect). SSRI starts → raphe 5-HT rises → autoreceptors brake firing → little net terminal 5-HT initially. Over ~2–4 weeks autoreceptors desensitise → firing recovers → terminal 5-HT rises → postsynaptic signalling. The classic account of the therapeutic delay. Buspirone is a 5-HT1A partial agonist (GAD).
- α2-adrenergic — autoreceptors on NE neurons + heteroreceptors on 5-HT terminals, both inhibitory. Mirtazapine antagonises them → disinhibits NE and 5-HT release.
- D2 — presynaptic autoreceptors (higher affinity, regulate DA release) vs postsynaptic. Aripiprazole/brexpiprazole/cariprazine are partial agonists ("dopamine stabilisers") — net antagonist where DA is high, net agonist where low.
- 5-HT2C — tonic inhibition of mesocortical DA/NE; antagonism (mirtazapine, several atypicals) disinhibits cortical monoamines.
- NMDA-on-interneurons — NMDA receptors sit on GABAergic interneurons; blocking them disinhibits pyramidal glutamate output. This sign-flip underlies both the schizophrenia NMDA-hypofunction model and ketamine's antidepressant action.
Master table — disorder × system × target × lever all disorders, with confidence tags▾
| Disorder | System(s) | Key receptors / targets | Putative mechanism / direction | Pharmacological lever | Confidence |
|---|---|---|---|---|---|
| Major depression | 5-HT, NE, DA; glutamate; GABA; neurotrophic | SERT, NET, DAT; 5-HT1A (auto + post), 5-HT2A/2C/7; α2 (auto); NMDA; AMPA; GABA-A (neurosteroid site); TrkB/BDNF | Monoamine "deficiency" (now seen as incomplete); newer: impaired synaptic plasticity / glutamatergic dysregulation; HPA-axis overdrive | SSRIs, SNRIs, bupropion, mirtazapine, agomelatine, ketamine/esketamine (NMDA→AMPA/mTOR), zuranolone/brexanolone (GABA-A PAM, PPD) | Rx MoA · H monoamine (weakening) · E glutamate/plasticity |
| GAD / anxiety | GABA, 5-HT, NE, Ca-channel | GABA-A (α2/α3 = anxiolysis, α1 = sedation); 5-HT1A (post); α2δ subunit of VGCC; locus coeruleus NE | GABAergic hypofunction / noradrenergic hyperreactivity | Benzodiazepines (PAM), buspirone (5-HT1A partial), SSRIs/SNRIs (first-line), pregabalin/gabapentin (α2δ) | Rx strong · H subtype-specific |
| Panic disorder | GABA, 5-HT, NE, respiratory chemosensitivity | GABA-A; 5-HT; locus coeruleus; CO₂/acid-sensing (false-suffocation model) | LC hyperexcitability + interoceptive misappraisal | SSRIs (first-line), benzodiazepines acutely | H |
| OCD | 5-HT, glutamate, DA | SERT (high-dose); cortico-striato-thalamo-cortical glutamate; D2 (striatal) | CSTC circuit hyperactivity; serotonergic modulation | High-dose SSRIs, clomipramine; antipsychotic augmentation (D2); glutamate modulators (memantine, riluzole — investigational) | Rx SSRI · E glutamate |
| PTSD | NE, HPA/glucocorticoid, 5-HT, glutamate | α1-adrenergic (post); glucocorticoid receptor; SERT; NMDA (fear extinction) | Noradrenergic hyperarousal; impaired extinction; HPA dysregulation | Prazosin (α1 antag — nightmares), SSRIs (sertraline, paroxetine); d-cycloserine (NMDA partial agonist) to augment exposure; MDMA-assisted therapy investigational | H · Rx prazosin |
| Schizophrenia | DA, glutamate, ACh, 5-HT | D2 (mesolimbic hyper → positive Sx; mesocortical hypo → negative/cognitive); 5-HT2A (post); NMDA-hypofunction on GABA interneurons; M1/M4 muscarinic; TAAR1 | Aberrant dopamine signalling downstream of glutamatergic/interneuron dysfunction | All antipsychotics block/partial-agonise D2; atypicals add 5-HT2A antagonism; xanomeline-trospium (M1/M4 agonist, no D2 action); ulotaront (TAAR1 — phase 3 mixed/negative) | Rx D2 blockade · H DA hypothesis · E NMDA/muscarinic |
| Bipolar — mania | DA; intracellular signalling | D2; GSK-3β; inositol monophosphatase (IMPase); Na/Ca channels | Dopaminergic hyperactivity; intracellular signalling/neuroprotection (lithium) | Lithium (multi-target, MoA uncertain), valproate, antipsychotics (D2), carbamazepine | ? lithium MoA · Rx antimanic effect |
| Bipolar — depression | mixed | as MDD + D2 partial agonism, 5-HT2A | — | Quetiapine, lurasidone, lamotrigine (Na-channel/glutamate), cariprazine | Rx/H |
| ADHD | DA, NE (prefrontal) | DAT, NET inhibition; α2A-adrenergic (post, PFC); D1/α2A tuning of PFC signal-to-noise | Hypodopaminergic/noradrenergic PFC; catecholamine "inverted-U" | Methylphenidate (DAT/NET block), amphetamine (release + reuptake), atomoxetine (selective NET), guanfacine/clonidine (α2A agonist) | Rx strong · H circuit model |
| Insomnia | GABA, orexin, melatonin, histamine | GABA-A (α1 = hypnotic); orexin OX1/OX2; MT1/MT2; H1 | Hyperarousal / wake-promoting orexin tone | Z-drugs & benzos (PAM), DORAs (suvorexant, lemborexant, daridorexant), ramelteon (MT agonist), sedating antihistamines/doxepin (H1) | Rx |
| Alcohol use | GABA, glutamate, opioid, DA | GABA-A; NMDA; µ-opioid; mesolimbic DA | Allostatic shift in reward + withdrawal hyperexcitability | Naltrexone (µ antag), acamprosate (glutamate/NMDA), disulfiram (ALDH — aversive); benzos for withdrawal | Rx |
| Opioid use | opioid, DA | µ-opioid (agonist/partial/antagonist) | Reward + dependence at µ receptor | Methadone (full agonist), buprenorphine (partial agonist), naltrexone (antagonist) | Rx |
| Nicotine use | cholinergic, DA | α4β2 nicotinic AChR; mesolimbic DA | Reward via nAChR-driven DA release | Varenicline (α4β2 partial agonist), bupropion, NRT | Rx |
| Dementia (AD) | ACh, glutamate; (amyloid) | Muscarinic/nicotinic via ↑ACh (AChE inhibition); NMDA (excitotoxicity); Aβ | Cholinergic deficit; glutamate excitotoxicity; amyloid cascade | Donepezil/rivastigmine/galantamine (AChE-I), memantine (NMDA antag), anti-amyloid mAbs (lecanemab, donanemab) | Rx symptomatic · H amyloid (contested) |
| Eating disorders | 5-HT, DA (limited) | SERT; D2 | Sparse; mostly empirical | SSRIs (bulimia/BED — fluoxetine, lisdexamfetamine for BED); olanzapine modest in anorexia | Weak H |
Caveats to keep handy for the viva▾
- The "chemical imbalance" framing is dead at the explanatory level. Receptor stories explain drug action and offer circuit-level hypotheses; they do not establish a deficiency/excess of a transmitter as cause. STAR*D, the collapse of the simple serotonin-depletion model, and the partial success of non-monoaminergic agents (ketamine, brexanolone, KarXT) all push this way.
- Receptor occupancy ≠ clinical effect ≠ etiology. D2 occupancy is near-immediate; antipsychotic response takes weeks — the gap is where the interesting biology (and most of the unknowns) lives.
- Net direction often inverts at the circuit. NMDA antagonism raising glutamate output, autoreceptor agonism lowering downstream tone, partial agonists behaving as functional antagonists in high-tone states.
- Newest agents are the tell. That muscarinic (KarXT), orexin, and neurosteroid mechanisms now work is a direct rebuke to single-transmitter models.
IIIDrug classes (core reference)
Per class: mechanism, indications, signature adverse effects, key monitoring, major interactions. Doses are never asserted in the scaffold — they live in SmPC / Maudsley slots. Mood stabilisers (lithium) carries the worked drug exemplar.
Antidepressants
| Class / drug | Mechanism · signature effects · monitoring |
|---|---|
| SSRIs | Serotonin reuptake inhibition. GI upset, sexual dysfunction, early activation/anxiety, hyponatraemia (esp. elderly), bleeding risk (with NSAIDs/anticoagulants), discontinuation. Citalopram/escitalopram: dose-dependent QTc (Part IV). |
| SNRIs (venlafaxine, duloxetine) | 5-HT + NE reuptake inhibition. As SSRIs plus dose-related BP rise (venlafaxine), pronounced discontinuation; useful in pain/anxiety. |
| TCAs | Reuptake inhibition + antimuscarinic/antihistaminic/α1 actions. Anticholinergic load, sedation, orthostasis, cardiotoxicity, dangerous in overdose. Largely second-line. |
| MAOIs | Monoamine-oxidase inhibition. Powerful but need the tyramine-free diet and serotonergic washouts (Part IV). Specialist/reserved. |
| Mirtazapine | α2 antagonist + 5-HT2/5-HT3 + H1 block. Sedation, weight gain; less sexual dysfunction/GI upset. |
| Bupropion | NA–DA reuptake inhibition. Activating, weight-neutral, low sexual dysfunction; lowers seizure threshold (avoid in eating disorders/seizure risk); CYP2D6 inhibitor. |
| Agomelatine | Melatonergic agonist + 5-HT2C antagonist. Sleep benefit, weight-neutral; hepatotoxicity — LFT monitoring. |
| Vortioxetine | Multimodal serotonergic; possible cognitive benefit; dose-related nausea. |
Add start/target doses, cross-taper/switch tables, washouts.
Antipsychotics · worked exemplar (clozapine)
FGAs are largely D2 antagonists → effective on positive symptoms but high EPS/prolactin. SGAs add 5-HT2A antagonism (+ varied H1/M1/α) → less EPS, more metabolic burden. Adverse signature follows the fingerprint: D2 → EPS/prolactin; H1/5-HT2C → weight; M1 → anticholinergic; α1 → orthostasis.
| Agent (examples) | Profile note |
|---|---|
| Haloperidol (FGA) | High-potency D2 → marked EPS, prolactin; QTc awareness. |
| Olanzapine | High metabolic burden; sedating; low EPS. |
| Risperidone / paliperidone | Dose-dependent EPS; most prolactin-raising SGAs. |
| Quetiapine | Sedating, low EPS/prolactin; metabolic & orthostatic effects. |
| Aripiprazole / cariprazine | D2 partial agonists → low metabolic/prolactin; akathisia/activation. |
| Clozapine | Most effective in treatment resistance; unique risks → worked exemplar below & Part IV. |
Add oral/depot doses, dose equivalents, LAI intervals.
Clozapine
SmPC via ↗ ANMDMR / ↗ EMA · red flags & monitoring §IV clozapine · monitoring schedule §VII · CYP1A2/smoking lever in Part II
The only agent with evidence in treatment-resistant schizophrenia — reserved after two adequate antipsychotic trials fail (≥ one an SGA). Broad, relatively D2-sparing receptor profile (notably muscarinic, H1, α; low EPS, little prolactin rise) underlies both its efficacy and its adverse load. Its serious risks are consolidated in §IV · clozapine red flags and not repeated here: severe neutropenia/agranulocytosis (ANC monitoring — post-REMS scheme & thresholds in §IV), myocarditis (first weeks — fever/tachycardia/chest pain → check), gut hypomotility/ileus (the leading cause of death — constipation is an emergency, not a nuisance), lowered seizure threshold, and high metabolic burden. It is a major CYP1A2 substrate, so smoking status drives the level — stopping smoking can push levels toward toxicity (see Part II CYP1A2). Short half-life → always taper; abrupt cessation risks rebound psychosis / cholinergic rebound. Plasma-level monitoring (TDM) is integral, not optional. No doses asserted here.
Empty slot: starting dose, slow titration schedule, target plasma-level range, smoking-status and re-titration-after-a-break adjustments.
Example completed slot. e.g. "Take constipation seriously — prophylactic laxative, ask at every review; in the first weeks treat fever/tachycardia/chest pain as possible myocarditis and check troponin/CRP/ECG; if the patient stops or cuts down smoking, anticipate a rising level and reduce dose with TDM; after a missed run of doses, re-titrate from low — don't resume the previous dose." Replace with your own.
Mood stabilisers · worked exemplar (lithium)
Lithium
SmPC via ↗ ANMDMR / ↗ EMA · monitoring cross-ref §IV lithium toxicity
First-line for bipolar maintenance and a benchmark for relapse prevention; augments antidepressants in resistant depression. Narrow therapeutic window — target levels, sampling timing, and toxicity precipitants are consolidated in §IV · lithium levels & toxicity. Signature: fine tremor, polyuria/polydipsia, weight gain, hypothyroidism, long-term renal effects; teratogenic (cardiac/Ebstein risk).
Empty slot: starting dose, titration-by-level, carbonate vs citrate, renal/elderly adjustment.
Example completed slot. e.g. "Check level 5–7 days after any dose change and ~12 h post-dose; counsel on hydration / NSAID avoidance; U&E/TFT/Ca²⁺ 6-monthly; review in pregnancy planning." Replace with your own.
Valproate · lamotrigine · carbamazepine
| Drug | Signature · monitoring · interactions |
|---|---|
| Valproate | Broad efficacy but highly teratogenic + neurodevelopmental risk — contraindicated in pregnancy and restricted in women of childbearing potential (pregnancy-prevention programme; check ANMDMR/EMA). Weight, tremor, hepatotoxicity, thrombocytopenia, pancreatitis; raises lamotrigine. |
| Lamotrigine | Best for bipolar depression/maintenance. Slow titration to avoid serious rash / SJS-TEN; dose interacts with valproate (↑) and inducers (↓). |
| Carbamazepine | Strong CYP3A4 inducer (many interactions); hyponatraemia, blood dyscrasias, rash (HLA-B*1502 in some ancestries); levels monitored. |
Add doses, valproate/carbamazepine level ranges, lamotrigine titration schedule.
Anxiolytics & hypnotics
| Drug/class | Note |
|---|---|
| Benzodiazepines | GABA-A modulation → rapid anxiolysis/sedation; tolerance, dependence, withdrawal (incl. seizures), falls/cognition in elderly, respiratory depression with opioids/alcohol. Short-term/crisis use. |
| Z-drugs (zolpidem, zopiclone) | Benzodiazepine-like hypnotics; similar dependence / next-day impairment. |
| Buspirone | 5-HT1A partial agonist; non-sedating, non-dependent; slow onset; GAD. |
| Pregabalin | α2δ calcium-channel modulator; GAD/neuropathic pain; misuse/dependence potential, sedation, weight. |
Add doses and your benzodiazepine-withdrawal taper schedule.
ADHD agents
| Drug/class | Note |
|---|---|
| Stimulants (methylphenidate, lisdexamfetamine) | DA/NA enhancers; first-line efficacy. Appetite/weight, sleep, BP/HR rise (baseline + monitoring), tics, mood; controlled drugs — check Romanian scheduling/availability; cardiac-history screening. |
| Atomoxetine | Selective NA reuptake inhibitor; non-stimulant; slower onset; BP/HR, hepatic, suicidality monitoring. |
| Guanfacine | α2A agonist; non-stimulant; sedation, hypotension/bradycardia. |
Add doses, titration, your cardiovascular monitoring proforma, Romanian availability.
IVHigh-yield safety & emergencies
Thresholds and intervals below are cited to current sources; confirm against the SmPC / Maudsley before acting. Each topic keeps a slot for your local protocol.
Emergency red-flag index▾
A fast triage index into the folds below. Fever + rigidity + raised CK on an antipsychotic → NMS → SS vs NMS. Clonus, hyperreflexia, agitation on a serotonergic → serotonin syndrome → SS vs NMS. Coarse tremor, ataxia, confusion on lithium → lithium toxicity → Lithium. Confusion + ataxia + ophthalmoplegia in alcohol use → Wernicke’s → Wernicke / DTs. Stupor, mutism, waxy flexibility → catatonia → Catatonia. Acute sustained eye/neck/tongue spasm on an antipsychotic → acute dystonia → EPS. Inner restlessness/pacing, new distress or suicidality → akathisia → EPS. New confusion/seizure + low sodium on an SSRI (elderly) → hyponatraemia/SIADH → Hyponatraemia. Falling phosphate on re-nutrition → refeeding → Refeeding. Fever/tachycardia/chest pain in the first weeks of clozapine → myocarditis → Clozapine.
Serotonin syndrome vs neuroleptic malignant syndrome▾
In someone on a serotonergic agent, diagnose if any of: spontaneous clonus; inducible clonus with agitation or diaphoresis; ocular clonus with agitation or diaphoresis; tremor with hyperreflexia; or hypertonia with temperature > 38 °C plus ocular or inducible clonus. Neuromuscular signs dominate (more marked in the legs). Onset within hours; resolves fast on stopping the agent. Manage: stop all serotonergic drugs, benzodiazepines, supportive care. (Hunter Serotonin Toxicity Criteria — Dunkley/Buckley, QJM 2003; sens 84% / spec 97%.)
On a dopamine antagonist (or after dopaminergic withdrawal): lead-pipe rigidity, hyperthermia, autonomic instability, altered consciousness, markedly raised CK. Onset over days to weeks (slower than serotonin syndrome). Manage: stop the antipsychotic, supportive care, ± dantrolene / bromocriptine; specialist input.
| Feature | Serotonin syndrome | NMS |
|---|---|---|
| Trigger | serotonergic drug | dopamine antagonist / DA withdrawal |
| Onset | hours | days–weeks |
| Neuromuscular | clonus, hyperreflexia (hyperkinetic) | lead-pipe rigidity, bradykinesia |
| Resolution | rapid on withdrawal | slow |
↗ StatPearls — Serotonin Syndrome
Add your escalation/management steps and who to call.
Lithium: levels & toxicity▾
Maintenance serum lithium 0.6–0.8 mmol/L (up to 1.0 if prior relapse / residual symptoms); acute mania often targeted 0.8–1.0. Toxicity is an emergency above ~1.5 mmol/L, with caution from ~1.2 (older patients may show toxicity near 1.0). Sample 12 h post-dose. Early toxicity: coarse tremor, GI upset, ataxia, dysarthria, confusion → seizures, renal failure. Precipitants: dehydration, NSAIDs, ACE-i/ARB, thiazides, infection. (NICE CG185; Maudsley — verify current edition.)
↗ NICE — mental health guidance
Add local toxicity management and dialysis-referral criteria.
Extrapyramidal effects & tardive dyskinesia▾
| Syndrome | Picture & timing |
|---|---|
| Acute dystonia | Sustained spasm (oculogyric crisis, torticollis) — hours to days; anticholinergic; can be dangerous (laryngeal). |
| Akathisia | Subjective inner restlessness + need to move — easily missed, linked to distress/suicidality; reduce dose / switch / consider propranolol. |
| Parkinsonism | Bradykinesia, rigidity, tremor — weeks; dose reduction / switch. |
| Tardive dyskinesia | Late, often irreversible choreoathetoid movements — months–years; minimise exposure, review, specialist options (VMAT2 inhibitors). |
Acute dystonia: sudden sustained spasm (oculogyric crisis, torticollis, trismus, tongue protrusion) within hours–days of starting or increasing a (usually high-potency) antipsychotic — or an antiemetic (metoclopramide, prochlorperazine); commoner in young men. Laryngeal/pharyngeal dystonia can threaten the airway — treat urgently with a parenteral anticholinergic (procyclidine or biperiden IM/IV), with rapid relief. Akathisia: a subjective inner restlessness with an irresistible urge to move — under-recognised and often mistaken for agitation or worsening psychosis, prompting the harmful reflex of increasing the antipsychotic. It is linked to distress, suicidality, and aggression, so it matters. Manage by reducing the dose or switching to a lower-propensity agent; adjuncts with some evidence include propranolol and mirtazapine, with short-term benzodiazepines. Distinguish from psychomotor agitation and from restless legs. (Paraphrased; Maudsley — verify edition.)
Add your EPS rating-scale routine and management ladder.
Antidepressant discontinuation & anticholinergic toxicity▾
On stopping/reducing (esp. short-t½ SSRIs/SNRIs — paroxetine, venlafaxine): flu-like symptoms, "brain zaps", dizziness, insomnia, mood/irritability — typically within days, self-limiting, eased by slower taper. Distinguish from relapse (later onset, full syndrome).
From cumulative antimuscarinic load (TCAs, low-potency antipsychotics, anticholinergics): "hot, dry, red, blind, mad" — hyperthermia, dry skin/mouth, flushing, blurred vision, urinary retention, delirium; tachycardia. Watch cumulative burden in the elderly (cognition, falls).
Add your tapering schedules and a cumulative anticholinergic-burden tool.
Antipsychotic metabolic monitoring▾
Baseline: weight/BMI, waist, BP, fasting glucose or HbA1c, lipids (+ prolactin if symptomatic). Then re-check at about 12 weeks, then at least annually — weight tracked more often early (NICE: weekly for the first weeks on some agents). Olanzapine and clozapine carry the highest metabolic burden. (NICE; Maudsley; ADA/APA 2004 consensus — verify current edition.)
Add your clinic's metabolic-monitoring sheet / recall system.
QTc prolongation▾
QTc is prolonged above ~450 ms (men) / 470 ms (women); > 500 ms — or an increase of > 60 ms from baseline (verify against AHA/ACC/ESC) — marks high torsades-de-pointes risk. Higher-risk psychotropics include high-dose/IV haloperidol, citalopram/escitalopram (dose-dependent), and some TCAs; risk multiplies with hypokalaemia/hypomagnesaemia, bradycardia, and other QT-prolonging drugs. (CredibleMeds clinical overview; FDA E14.)
↗ CredibleMeds — long-QT/TdP overview (drug lists need free registration)
Add agent-specific cautions and your pre-/on-treatment ECG rules.
Clozapine red flags & monitoring▾
FBC with ANC weekly for the first 18 weeks → fortnightly to week 52 → every 4 weeks thereafter (and 4 weeks after stopping). UK/EU thresholds: green ANC ≥ 2.0; amber 1.5–2.0 (increase monitoring); red < 1.5 (stop); agranulocytosis < 0.5 (×10⁹/L). Follow the SmPC + the national/manufacturer monitoring service. (SmPC; Maudsley.)
Myocarditis (esp. first ~4–8 weeks — troponin/CRP, tachycardia, chest pain, fever); ileus / severe constipation (GI hypomotility, can be fatal — ask actively); dose-related seizures; pneumonia; sialorrhoea; smoking cessation raises levels (CYP1A2).
Add the Romanian monitoring-service detail and your rechallenge/registration process.
MAOI precautions▾
Tyramine: with non-selective MAOIs, tyramine-rich foods (aged cheese, cured meats, some fermented products, tap/draught beer) risk a hypertensive crisis — dietary counselling is mandatory. Serotonergic washout: strict drug-free intervals before/after MAOIs and other serotonergic agents (incl. the long washout after fluoxetine, and "hidden" serotonergic drugs — linezolid, methylene blue, tramadol, pethidine) to avoid serotonin syndrome. Follow the SmPC/Maudsley for exact washout periods.
Add exact washout intervals and a patient-facing food list.
Wernicke’s encephalopathy & delirium tremens (alcohol)▾
A thiamine-deficiency emergency in alcohol dependence (also hyperemesis, post-bariatric, malnutrition). The classic triad — confusion, ataxia, ophthalmoplegia/nystagmus — is fully present in only a minority, so treat on suspicion. Give parenteral thiamine before any glucose (a glucose load without thiamine can precipitate it). Low threshold, generous parenteral dosing, then oral continuation; untreated it progresses to Korsakoff’s (largely irreversible anterograde amnesia with confabulation). (Paraphrased; verify doses against the SmPC / local protocol — RO: tiamină injectabilă.)
The severe end of alcohol withdrawal, typically ~48–72 h after the last drink: clouding of consciousness, disorientation, vivid hallucinations, a marked autonomic storm (tachycardia, hypertension, fever, diaphoresis), and tremor — a medical emergency with real mortality. Withdrawal seizures usually come earlier (~6–48 h). Manage with benzodiazepines (symptom-triggered or fixed-dose per CIWA-Ar / local protocol), fluids and electrolytes, and thiamine, in a setting able to escalate. Higher risk with prior DTs/seizures, heavy intake, and comorbidity.
↗ StatPearls — Wernicke encephalopathy
Add your unit’s parenteral thiamine regimen and symptom-triggered benzodiazepine protocol.
Catatonia▾
A psychomotor syndrome — not specific to schizophrenia; it is common in mood disorders and in medical/neurological illness. Features include stupor, mutism, negativism, posturing, waxy flexibility, catalepsy, echophenomena, stereotypy, and excitement. Screen with the Bush–Francis scale, and always look for a medical/organic cause.
A lorazepam challenge (a test dose, watching for partial relief) is both diagnostic and therapeutic; benzodiazepines are first-line and ECT is definitive, especially when severe or refractory. Avoid first-line antipsychotics — they can worsen catatonia and raise the risk of malignant catatonia / NMS.
Add your screening routine and the local lorazepam-challenge / ECT pathway.
SSRI/SNRI hyponatraemia & SIADH▾
SSRIs and SNRIs can cause hyponatraemia through SIADH, usually in the first few weeks; risk rises with age, female sex, low body weight, diuretics, and other hyponatraemia-causing drugs. It is easily missed because the symptoms — lethargy, confusion, headache, falls, and at the severe end seizures — are nonspecific and get read as “the depression” or “ageing.” Check sodium if a newly started older patient becomes confused or falls. Manage by stopping/switching the agent, fluid restriction, and correcting sodium slowly (over-rapid correction risks osmotic demyelination); mirtazapine is sometimes chosen as a lower-risk switch. (Paraphrased; verify against the SmPC.)
Add your baseline/early sodium-check routine and safe correction-rate limits.
Refeeding syndrome▾
When a starved or severely malnourished patient is fed, the insulin surge drives phosphate, potassium, and magnesium into cells → hypophosphataemia (the hallmark), hypokalaemia, hypomagnesaemia, thiamine depletion, and fluid shifts → arrhythmia, cardiac failure, seizures, death. Highest risk in anorexia nervosa and prolonged undernutrition (cross-reference the eating disorders card). Prevent: identify risk, start low and go slow with calories, give thiamine and replace electrolytes before/with feeding, and monitor phosphate/potassium/magnesium closely over the first days. (Paraphrased; follow a risk framework — MEED / NICE / local protocol; verify current edition.)
Add your refeeding risk-stratification and the daily electrolyte-monitoring schedule.
VAssessment & examination
The mental state examination as a structured cross-section of current state, a risk-assessment framing, and an orientation to where rating scales fit. Orientation only — confirm against your local proforma and policy.
The mental state examination (MSE) is a structured snapshot of the patient’s presentation at the moment of assessment — the psychiatric equivalent of the physical exam. It records what is observed (appearance, behaviour, speech, affect) and what is elicited (mood, thought, perception, cognition, insight), separately from the history. It is descriptive, not a checklist to be scored, and not a diagnosis in itself. The scaffolds below name the domains and what each captures; your service’s own proforma and the wording of any instrument live in the slot. Cross-check structure against an open reference such as StatPearls — Mental Status Examination.
Mental state examination
The observable, before a word is exchanged: apparent vs stated age, build, self-care and grooming, dress (appropriate to setting/weather?), distinguishing features, signs of physical illness or substance use, objects carried. Records the baseline a later assessor can compare against.
Engagement and rapport, eye contact, level of motor activity (retardation vs agitation/restlessness), abnormal movements (tremor, tics, tardive dyskinesia, catatonic signs), psychomotor signs of arousal or distress, and whether behaviour is appropriate and cooperative. Note any responding-to-unseen-stimuli.
The form of talk, not its meaning (that is thought): rate, rhythm, volume, quantity, spontaneity, tone, and articulation. Pressured/rapid vs slowed/poverty of speech; latency of response; dysarthria or dysphasia. Content is recorded under thought.
Mood is the sustained, subjectively reported emotional state (the patient’s own words, quoted, plus your rating). Affect is the observed, moment-to-moment emotional expression: its range/reactivity (full, restricted, blunted, flat), appropriateness/congruence to thought, and stability (labile?). Note the relationship between the two.
The structure and flow of thinking, inferred from speech: tempo (flight of ideas, retardation) and connectedness (circumstantiality, tangentiality, loosening of associations / derailment, word salad, perseveration, thought block, neologisms). Describes how thoughts are linked, separately from what they contain.
What is on the patient’s mind: preoccupations and overvalued ideas; obsessions and compulsions; delusions (fixed false beliefs — persecutory, grandiose, nihilistic, reference, control, guilt) and how firmly held; abnormal beliefs about thought possession (insertion, withdrawal, broadcast); and a recorded screen for suicidal, self-harm and harm-to-others ideation (cross-refers to risk, below).
Abnormal percepts by modality: hallucinations (auditory — including second/third-person and commentary — visual, olfactory, gustatory, somatic/tactile), illusions, and altered perception of self/surroundings (depersonalisation, derealisation). Note whether the patient has insight into them and any link to mood.
A bedside screen, not a formal neuropsychological battery: level of consciousness, orientation (time/place/person), attention and concentration, short-term and working memory, and obvious language/executive difficulty. Flag anything suggesting delirium or an organic cause for formal testing. See the cognitive-screen pointer below.
Insight is graded, not binary: awareness that something is wrong, that it is a mental-health problem, that treatment may help, and willingness to accept it. Judgement is the capacity to reason through situations and consequences — best evidenced by recent real decisions rather than hypothetical scenarios. Both bear directly on capacity and risk.
When the cognitive domain raises concern, a structured screen is used rather than impression alone — e.g. MMSE, MoCA, or the AMT/AMT-10 for rapid bedside use. These are instruments: their items, scoring and cut-offs are set out (with licensing) in the rating-scales table below — not reproduced here. A screen flags the need for, but does not replace, formal cognitive assessment where an organic cause is suspected.
Risk assessment
Risk assessment is a structured clinical judgement, not a predictive score — instruments support but never substitute for it, and a low “score” never overrides clinical concern. Assess and document across three axes: (1) risk to self — suicidal ideation/intent/plan/means/preparatory acts, history of attempts, self-harm; (2) risk to others — thoughts/intent to harm, history of violence, identified targets, command hallucinations; (3) risk from others / safeguarding — self-neglect, vulnerability, exploitation or abuse, and risk to dependents. For each: current state, static and dynamic factors, protective factors, and an explicit management plan. Reassess on change — risk is dynamic.
The MSE and risk formulation are only as useful as their handover. Record contemporaneously and in descriptive terms (what was observed/said, ideally quoted), not interpretation alone. A structured handover idiom — SBAR (situation, background, assessment, recommendation) — carries the picture safely between clinicians and shifts. Where the assessment turns on whether the patient can consent to or refuse assessment/treatment, that is a capacity question — see the legal & capacity orientation (Part VII).
↗ StatPearls — Mental Status Examination · ↗ StatPearls — Suicide Risk Assessment · ↗ WHO — Mental Health
Drop in your service’s MSE proforma, risk-assessment template and escalation/safeguarding pathway, and any locally-mandated instrument and its cut-offs.
Rating-scales pointer table
What each common instrument is for and how to obtain it — not the items themselves, which are copyrighted or licensed and belong in the source, not here. Use this to pick the right tool and find its official source; record your local cut-offs in the slot. A scale supports clinical judgement; it does not replace it.
| Instrument | What it measures | Format · where it fits | Access & licensing |
|---|---|---|---|
| PHQ-9 | Depression severity & monitoring; tracks symptom change over treatment. | 9-item self-report; primary care & general screening. | Free — Pfizer placed it in the public domain (2010); no permission to reproduce/translate/distribute. phqscreeners.com |
| GAD-7 | Generalised-anxiety severity (also screens panic/social/PTSD). | 7-item self-report; primary care & general screening. | Free — same Pfizer 2010 release; no permission required. phqscreeners.com |
| HAM-D (HDRS) | Clinician-rated depression severity; long-standing trial standard. | Clinician-administered (17/21-item versions). | Widely available, free to use in clinical/research practice; versions vary — cite the version you use. |
| MADRS | Clinician-rated depression severity; sensitive to change, light on somatic items. | 10-item clinician-administered. | Widely available and freely used in practice; obtain the official form from a primary source. |
| YMRS | Mania severity & treatment response. | 11-item clinician-rated. | Widely reproduced and freely used clinically; cite source. |
| PANSS | Positive, negative & general psychopathology in psychotic illness. | 30-item clinician interview-based; requires rater training. | Copyrighted/licensed — obtain through the publisher (distributed via Multi-Health Systems); rater training expected. |
| MMSE | Global cognitive screen (orientation, registration, recall, language). | 30-point clinician-administered. | Proprietary since 2000 — licensed via PAR (Psychological Assessment Resources); purchase/permission required. |
| MoCA | Cognitive screen more sensitive to mild impairment than MMSE. | 30-point clinician-administered. | Copyrighted; mandatory training/certification to administer (free for students/academia/public-health; fee for commercial use). mocatest.org |
| AUDIT | Hazardous/harmful alcohol use & possible dependence. | 10-item; self-report or interview. | WHO instrument — free to use; manual downloadable from WHO. |
| Bush–Francis (BFCRS) | Catatonia — screening & severity. | Clinician-rated (screening subset + full scale). | Freely available in the clinical literature; cite the source publication. |
| CIWA-Ar | Alcohol-withdrawal severity; drives symptom-triggered benzodiazepine dosing. | 10-item clinician-rated, serial use. | Freely available and widely reproduced in clinical protocols. |
↗ PHQ / GAD-7 (Pfizer, free) · ↗ AUDIT (WHO) · ↗ MoCA · ↗ MMSE (PAR)
Record the version/language you use, its validated cut-offs for your population, and any local administration/scoring protocol. Do not paste copyrighted item content into this file — keep it in your licensed source.
Score calculators — free scales
Interactive companions to the pointer table above, for the instruments that are public-domain or free to reproduce. Each takes the item values you read from your own validated copy and returns a running total and interpretation band. Licensed instruments (MMSE, MoCA, PANSS) have no calculator — only the reference links above. A score supports clinical judgement; it never replaces it.
These calculators are an orientation aid, not a clinical authority. A total supports but never replaces clinical judgement, and no band here is diagnostic or decisive on its own. Confirm scoring, version and cut-offs against the validated instrument and your local policy before acting. Where a score touches risk — PHQ-9 item 9, withdrawal severity — treat the number as a prompt to assess, never as reassurance.
↑ PHQ-9 / GAD-7 (Pfizer, free) · ↑ AUDIT (WHO)
VITreatment algorithms by condition
The shape of each pathway only — for the actual stepwise algorithms use the linked sources, and reconcile drug choice/dose with the Romanian SmPC. Jurisdiction is labelled; add your local pathway in each slot.
↗ Psychopharmacology Algorithm Project · ↗ NICE (UK) · ↗ CANMAT (Canada) · ↗ BAP (UK)
Depression▾
Confirm diagnosis & screen for bipolarity → first-line antidepressant (SSRI usual) at adequate dose/duration → assess response/adherence → switch (within/across class) or, for partial response, augment (e.g. lithium, an atypical antipsychotic) → treatment-resistant: review diagnosis/adherence, consider esketamine/ECT per access. Psychotherapy throughout. (CANMAT 2023/2024; NICE.)
Confirm depression and grade severity (NG222: less severe vs more severe, ~PHQ-9 16 cut), assess suicide risk, and screen for bipolarity and substances before any antidepressant. Offer a menu of options: for less severe, guided self-help or psychological therapy may suffice; for more severe, combine an antidepressant with psychological therapy. Psychological therapy runs throughout.
Start an SSRI (choice led by tolerability, interactions, prior response) at an adequate dose. Warn about the first 1–2 weeks; review early (sooner if < 30 or higher suicide risk). Reassess at about 4 weeks (6–8 for fuller effect), having checked adherence: adequate response, partial response, or none?
Continue the effective antidepressant at the same dose for at least 6 months after remission (longer — often ≥ 2 years — with recurrent episodes or residual symptoms). Stopping early is a common relapse cause; taper to limit discontinuation symptoms.
First optimise the dose within tolerability. If still partial, augment — evidence-based options include lithium, an atypical antipsychotic (e.g. aripiprazole, quetiapine), or combining with mirtazapine. Reassess after an adequate interval.
Re-check adherence and the diagnosis, then switch — to another SSRI or, commonly, a different class (SNRI, mirtazapine, vortioxetine). Cross-taper as appropriate and give the new agent an adequate trial.
Inadequate response to ≥ 2 adequately dosed/timed trials → specialist input. Consider further augmentation/combinations, ECT (severe, psychotic, urgent, or food/fluid refusal), and esketamine where access permits. Re-confirm diagnosis and contributors (e.g. thyroid, substances, psychosocial).
Add your step order, augmentation choices/doses, referral points.
Bipolar disorder▾
Acute mania: antipsychotic and/or lithium or valproate; stop antidepressants. Bipolar depression: evidence favours specific agents (e.g. quetiapine, lurasidone, lamotrigine) over antidepressant monotherapy. Maintenance: lithium is the benchmark. Avoid valproate in women of childbearing potential. (CANMAT/ISBD 2018 + 2023 update.)
Confirm bipolar disorder and identify the phase — the pathway differs completely by phase. Universals: stop antidepressant monotherapy; baseline thyroid/renal function before lithium; and the valproate pregnancy-prevention programme (avoid valproate in women/girls of childbearing potential, ANM/EU).
First-line monotherapy: lithium, valproate (not in women of childbearing potential), or an atypical antipsychotic (e.g. quetiapine, aripiprazole, risperidone, olanzapine, asenapine, cariprazine). For severe mania, combine a mood stabiliser with an antipsychotic. Reassess response.
Switch to or add an alternative first-line agent (a different antipsychotic, or add/optimise lithium/valproate). Consider ECT for severe, treatment-resistant, or pregnancy cases. Then move to maintenance once stabilised.
Evidence favours specific agents over antidepressant monotherapy: quetiapine, lurasidone (± lithium/valproate), lithium, lamotrigine, or cariprazine. Antidepressants, if used at all, only alongside an antimanic agent and never as monotherapy (mood-switch / cycling risk). If inadequate, switch among these first-line options or seek specialist input, then maintain.
Continue the agent that achieved control; lithium is the benchmark (and the only agent with consistent anti-suicidal evidence). Tailor to predominant polarity (e.g. lamotrigine for depressive poles; some antipsychotics for manic poles). Monitor lithium level, renal and thyroid function; sustain psychoeducation and relapse planning.
Add agent choices/doses for mania, bipolar depression, maintenance.
Schizophrenia▾
Single antipsychotic at adequate dose/duration, chosen on adverse-effect profile and preference → if inadequate, switch to a second monotherapy → two adequate trials failing defines treatment resistance → clozapine (Part IV monitoring). Address adherence (consider long-acting injectables) and comorbid substance use throughout. (NICE; Maudsley.)
Offer a single antipsychotic (SGA or FGA) at the lowest effective dose, chosen on adverse-effect profile and patient preference, with psychological intervention (CBT for psychosis and family intervention). Do baseline metabolic and ECG/physical checks first (see metabolic monitoring).
Treat at a therapeutic dose for an adequate period (~4–6 weeks), then assess response, adherence, and tolerability.
Address adherence first (consider a long-acting injectable) and comorbid substance use, then switch to a different antipsychotic and give it an adequate trial.
Failure of two adequate antipsychotic trials (at least one an SGA) defines treatment resistance → offer clozapine, with its mandatory haematological and physical monitoring (see clozapine red flags). For partial clozapine response, specialist augmentation strategies follow.
Continue the effective antipsychotic at the lowest effective dose; emphasise relapse prevention, adherence (LAI where helpful), and ongoing physical-health monitoring (see metabolic monitoring).
Add trial-duration definitions, LAI choices, clozapine-initiation route.
Anxiety / OCD▾
First-line: SSRI/SNRI + CBT (exposure-based for OCD/phobias). OCD often needs higher doses and longer trials; partial response → switch SSRI, then consider clomipramine or antipsychotic augmentation. Avoid routine long-term benzodiazepines. (NICE; BAP.)
Psychoeducation and stepped care for all; CBT is central — exposure-based, with ERP for OCD and phobias. Then pick the pharmacological track.
First-line SSRI (or SNRI); start low to avoid early activation, and allow a longer trial (~6–12 weeks) than in depression. Partial/no response → switch SSRI/SNRI, then consider pregabalin (GAD). Avoid routine long-term benzodiazepines (short-term, crisis use only).
First-line SSRI, typically at higher doses and a longer trial (~10–12 weeks), with CBT/ERP. Inadequate → switch SSRI or try clomipramine; augment with an antipsychotic in resistant cases; specialist referral.
Add dosing ceilings, trial lengths, augmentation steps.
ADHD▾
Confirm diagnosis + baseline cardiovascular screen → stimulant first-line (methylphenidate or lisdexamfetamine), titrated to response/tolerability → non-stimulant (atomoxetine, guanfacine) where stimulants unsuitable → treat comorbidities. Monitor BP/HR, weight, sleep, mood. Confirm Romanian scheduling/availability. (NICE; BAP.)
Confirm the diagnosis and do a baseline cardiovascular assessment (pulse, blood pressure; ECG if a cardiac history/indication), height and weight. Add psychoeducation and environmental/behavioural support. Then choose by age.
First-line methylphenidate; if an adequate trial is inadequate, switch to lisdexamfetamine (then dexamfetamine). Use a non-stimulant (atomoxetine or guanfacine) where stimulants are ineffective, not tolerated, or unsuitable.
First-line lisdexamfetamine or methylphenidate; switch between them if one is ineffective after an adequate trial. Atomoxetine where stimulants are unsuitable, not tolerated, or where diversion risk is a concern.
Titrate to response and tolerability; monitor growth (children), pulse/BP, sleep, appetite, mood and tics. Treat comorbidities. Confirm Romanian scheduling/availability and arrange shared care.
Add titration, shared-care arrangements, Romanian availability notes.
VIISpecial populations & monitoring
Pregnancy & lactation
↗ UKTIS / "bumps" (pregnancy) · ↗ LactMed (lactation) · ↗ EMA / SmPC (EU)
Decisions weigh the risk of untreated illness against medication risk, individualised and shared. Valproate is contraindicated in pregnancy and restricted in women of childbearing potential (pregnancy-prevention programme — check ANMDMR/EMA). Lithium carries first-trimester cardiac risk (Ebstein's) and needs careful peripartum level management. Use UKTIS/bumps + LactMed + the SmPC for drug-specific data; verify per case.
Add your preferred agents by trimester and the local perinatal-psychiatry route.
Older adults · renal/hepatic impairment · children & adolescents
Older adults: "start low, go slow"; anticholinergic burden, falls, hyponatraemia, QTc, and antipsychotic stroke/mortality risk in dementia. Renal/hepatic impairment: dose-adjust per SmPC (lithium is renally cleared — caution; many agents need hepatic adjustment). Children/adolescents: narrower evidence base and licensing; specialist initiation; monitor for activation/suicidality on antidepressants.
Add renal/hepatic dose adjustments and paediatric specifics you use.
Consolidated monitoring schedules
| Drug | Core monitoring (verify against SmPC / NICE / Maudsley) |
|---|---|
| Lithium | Level 12 h post-dose (weekly until stable, then ~3-monthly); U&E/eGFR + TFTs + Ca²⁺ ~6-monthly; weight. |
| Clozapine | FBC/ANC weekly ×18 wk → fortnightly to 1 yr → 4-weekly; plus metabolic, cardiac (myocarditis early), GI (constipation), levels prn. |
| Antipsychotics (all) | Metabolic panel baseline → ~12 wk → annually; weight more often early; prolactin if symptomatic; ECG where QTc risk. |
| Valproate / carbamazepine | LFTs, FBC; levels where indicated; pregnancy-prevention (valproate); Na⁺ (carbamazepine). |
| Lamotrigine | Clinical rash vigilance during slow titration. |
Add your clinic's exact intervals and how recalls are tracked.
Legal & capacity orientation (Romania)
This is an orientation to Romanian law only, not legal advice, and it changes by amendment. Confirm every article number, threshold and time limit against the current consolidated text at the official portal before acting — the law has been amended as recently as 2024. Framework last verified Jun 2026 · ↗ legislatie.just.ro (consolidated)
The governing statute is the Mental Health Act — Legea sănătății mintale și a protecției persoanelor cu tulburări psihice nr. 487/2002 (republished in the Official Gazette, Sep 2012), with its application norms (Ministry of Health, 2016). Article 55 was amended in 2024 (Ordinance 18/2024, approved by Law 175/2024), broadening where involuntary admission may take place — so a memory of the older text will be wrong. Capacity and consent also engage the Civil Code, not only this Act. Paraphrased orientation throughout; consult the primary text for wording.
Voluntary admission works like admission to any other medical service, and the patient may request discharge at any time unless the conditions for continued involuntary detention are met. Involuntary admission is a last resort, applied only once voluntary options are exhausted, and only where a qualified psychiatrist judges a psychic disorder to be present together with either (a) imminent danger of harm to self or others, or (b) — in severe disorder — a likelihood that not admitting would cause serious deterioration or prevent appropriate treatment. Importantly, involuntary admission does not in itself restrict the patient's legal capacity.
| Step (orientation — confirm articles) | What happens |
|---|---|
| Grounds | Qualified psychiatrist finds a psychic disorder + imminent danger to self/others, or severe disorder where non-admission risks serious deterioration / denies needed treatment. |
| Who may request | Treating family doctor or psychiatrist; family; local public-administration / social-medical & public-order representatives; police, gendarmerie, firefighters, or prosecutor; the civil court during proceedings. |
| Evaluation & information duty | Psychiatrist evaluates without delay, informs the person and their legal representative of the treatment decision and of the involuntary-admission proposal, and forwards documentation to the review commission within a short statutory window. |
| Review commission | A specially constituted commission (paraphrased: three members — two psychiatrists plus another doctor or a civil-society representative) analyses the proposal within a short statutory deadline after examining the person where possible. |
| Court confirmation | The decision is referred to the civil court, judged urgently. Emergency admission by the psychiatrist is possible, with immediate notification of the person, their representative and the commission. |
| Rights during detention | Non-restrictable rights are protected — communication with authorities/family/representative/lawyer, personal correspondence and private phone use, press access, the vote (unless otherwise restricted), and free religious practice. |
Treatment generally requires the patient's consent; where capacity is impaired, the roles of legal and conventional/personal representatives come into play, as defined in the Act and the Civil Code. Capacity is decision-specific and situation-specific — it cross-refers directly to the MSE insight & judgement domain and is assessed for the decision at hand, not as a global label. Detention and capacity are separate questions: a person can be detained yet retain legal capacity.
Romanian practice sits under a wider frame: the ECHR Article 5 (right to liberty and security, governing lawful detention of persons of "unsound mind") and the UN CRPD (Convention on the Rights of Persons with Disabilities). These shape — but do not replace — the domestic procedure above; where national and supranational standards interact, take advice.
Add your hospital's involuntary-admission commission procedure and forms, the exact current article numbers and time limits, and a note of the statute version/date you last verified.
↗ Legea 487/2002 — consolidated (legislatie.just.ro) · ↗ Portal Legislativ (check for amendments)
+Brief orientation: therapies
Psychotherapies
CBT — structured, present-focused work on thoughts/behaviours (depression, anxiety, OCD with exposure, CBTp for psychosis). DBT — skills + validation for emotion dysregulation/self-harm (borderline pattern). IPT — interpersonal focus in depression. Others: psychodynamic, MBT, EMDR (trauma), family interventions (psychosis, eating disorders). Match modality to disorder and evidence; combine with pharmacotherapy where indicated.
Add what's accessible to your patients and how to refer.
ECT & neuromodulation
ECT — fastest, most effective option for severe/treatment-resistant depression, depression with high suicide risk or refusal to eat/drink, catatonia, and severe mania; main adverse effect is transient cognitive/memory impairment. rTMS — non-convulsive option in treatment-resistant depression. Other neuromodulation (VNS, DBS) is specialist/restricted. Follow NICE/local criteria and consent frameworks.
Add where ECT/rTMS is available and your consent/capacity process.
Orientation layer complete across Parts 0–VII+ · slots throughout await your book-deep detail (search @@EXPAND) · verify all doses, criteria, and interactions against current primary sources before any clinical decision