Psychiatry – Summative Revision Notes

DSM-5 dropped the bereavement exclusion, but grief and MDD remain distinguishable by symptom quality, not timing alone — intermittent vs. pervasive low mood, preserved vs. absent capacity for positive affect, presence or absence of true anhedonia and pathological guilt.

Hypomania = ≥4 days, observable change, no marked functional impairment, psychosis, or hospitalisation. Mania = ≥7 days or any hospitalisation, regardless of duration. Bipolar II requires hypomania plus a major depressive episode — never a full manic episode.

SSRI monotherapy in a bipolar patient — without a mood stabiliser or antipsychotic on board — carries a recognised risk of precipitating mania, hypomania, or a mixed episode. Concurrent depressive and manic/hypomanic symptoms together define mixed features.

Persistent depressive disorder (≥2 years, symptom-free gaps never exceeding 2 months) plus a superimposed major depressive episode can be coded together — DSM-5 does not treat these as mutually exclusive.

Escitalopram (Nexito, Cipralex) remains the most commonly reached-for SSRI starting point across mood and anxiety presentations alike — worth knowing the brand cold, since prescriptions and case vignettes both use it freely.

Grief ≠ MDD by timing alone — symptom quality decides Hypomania ≥4 days; mania ≥7 days or any hospitalisation SSRI monotherapy can switch a bipolar patient Atypical = reactive mood + hypersomnia; melancholic = the opposite

SSRI or SNRI (escitalopram, venlafaxine) is first-line. Buspirone (Buspin) is a non-habit-forming alternative. Benzodiazepines (alprazolam — Restyl, Alprax) may bridge the first weeks but are not maintenance therapy.

SSRI (paroxetine, sertraline) first-line; given its 2–4 week lag, a short-term benzodiazepine bridge — classically clonazepam (Petril, Clonotril) — is often co-prescribed and tapered once the SSRI takes hold.

OCD needs higher SSRI doses than depression (fluoxetine up to 60–80mg) and longer trials (8–12 weeks at the higher dose) before judging response. Clomipramine (Anafranil) — a TCA with potent serotonergic activity — is the recognised second-line option.

Sertraline and paroxetine carry the strongest evidence and are first-line. For nightmares specifically, prazosin (Minipress) — an alpha-1 blocker, repurposed from its antihypertensive role — has dedicated trial evidence.

Propranolol (Ciplar) is for performance-only social anxiety — a single dose before a discrete event like a viva or public talk. It is not maintenance therapy for generalised social anxiety, and it is not a mechanism-matched substitute for an SSRI.

GAD: SSRI/SNRI first-line, benzo bridges only OCD needs higher doses, longer trials than depression Prazosin targets PTSD nightmares specifically Propranolol = performance anxiety only, not daily use

Antipsychotic treatment starts promptly once active psychosis is identified — duration tiers guide eventual diagnosis and prognosis, not whether or when to begin treatment.

Needs a mood episode concurrent with psychosis for a substantial portion of the illness, plus ≥2 weeks of psychosis with no mood episode at all. That second clause is what separates it from mood disorder with psychotic features, where psychosis tracks only with mood episodes.

≥1 month, non-bizarre, functioning preserved outside the delusion's direct impact. Subtypes: erotomanic, persecutory, grandiose, jealous, somatic. Poor insight into the delusion itself often limits engagement with treatment — even while the patient functions well otherwise.

Thought broadcasting, thought insertion/withdrawal, somatic passivity, delusional perception — classically associated with schizophrenia, but DSM-5 gives them no special standalone diagnostic weight anymore. Same ≥2-symptom/duration/functional criteria apply regardless.

Haloperidol (Serenace) IM remains the standard for acute agitation in an undifferentiated psychotic presentation; risperidone (Risdone, Sizodon) is a common oral starting atypical once the acute phase settles.

Brief → schizophreniform → schizophrenia by duration Schizoaffective needs psychosis WITHOUT mood episode too Delusional disorder: functioning preserved outside the delusion First-rank symptoms: suggestive, not privileged, in DSM-5

Beyond the usual GI/sexual side effects, watch specifically for SIADH-related hyponatraemia — a clinically important, exam-favoured elderly-specific risk.

~5 weeks after fluoxetine (Fludac, Prozac) specifically — vs. ~2 weeks for other SSRIs — because norfluoxetine's long half-life risks serotonin syndrome if an MAOI is started too soon.

Coarse tremor + ataxia + confusion + vomiting → check serum lithium (Licab, Lithosun) urgently. In pregnancy, the teratogenic risk is cardiac — Ebstein's anomaly, not neural tube defects.

QRS >100ms = sodium channel blockade. IV sodium bicarbonate is the priority — not calcium gluconate, which is for calcium-channel-blocker toxicity, a different mechanism entirely. Amitriptyline (Tryptomer) is the classic culprit in deliberate overdose vignettes.

SSRIs in elderly: watch for SIADH/hyponatraemia Fluoxetine needs ~5-week MAOI washout Lithium + pregnancy = Ebstein's, not neural tube defect TCA overdose QRS widening → sodium bicarbonate

5-HT2A antagonism layered on D2 blockade disinhibits nigrostriatal dopamine, partially offsetting the D2 block — the core mechanistic reason atypicals (risperidone, olanzapine, quetiapine) carry lower EPS risk than typicals.

Orofacial movements after long-term typical antipsychotic use. Anticholinergics worsen, not treat, TD — that's the reverse of their role in acute EPS (see below). Valbenazine and deutetrabenazine (VMAT2 inhibitors) are the newer licensed options.

For acute drug-induced parkinsonism or dystonia — rigidity, tremor, shuffling gait soon after starting a typical antipsychotic — the standard agent is trihexyphenidyl (Tripax, Pacitane), an anticholinergic that restores the dopamine-acetylcholine balance disrupted by D2 blockade. The trap: this is the opposite drug class strategy from TD, where anticholinergics make things worse. Timing and movement type (parkinsonian vs. choreiform/orofacial) is what separates the two scenarios.

Reserved for treatment-resistant schizophrenia (failed ≥2 adequate trials). Agranulocytosis risk mandates weekly → fortnightly FBC monitoring. Clozapine (Clozapex, Sizopin) also carries the highest metabolic burden of any atypical, alongside olanzapine (Oleanz).

Quetiapine (Quitipin, Qutan) is sedating and frequently used off-label for insomnia or anxiety augmentation beyond its primary antipsychotic/mood-stabiliser-adjunct role — common in real prescriptions, worth recognising by brand.

Atypicals: 5-HT2A blockade offsets D2-driven EPS NMS = days + lead-pipe; serotonin syndrome = hours + clonus Anticholinergics: treat acute EPS, worsen TD Clozapine: treatment-resistant only, mandatory FBC monitoring

Seizures ~24–48h, delirium tremens ~48–72h post last drink. Chlordiazepoxide (Librium, Equilibrium) or diazepam first-line, symptom-triggered (CIWA-Ar) or fixed reducing schedule.

Confusion + ataxia + ophthalmoplegia. IV thiamine (Pabrinex) before or with glucose — glucose-first can precipitate or worsen Wernicke's in a thiamine-depleted patient.

Methadone = full agonist, real overdose risk, supervised dosing. Buprenorphine (often as Suboxone, with naloxone) = partial agonist, ceiling effect on respiratory depression, safer for take-home use; the naloxone component deters injection misuse.

~9% of ever-users, ~17% of daily users develop dependence. A recognised DSM-5 withdrawal syndrome exists too — the "cannabis isn't addictive" claim is factually incorrect.

Seizures ~24–48h, DTs ~48–72h after last drink Thiamine before glucose in suspected Wernicke's Naloxone for overdose, not for withdrawal Buprenorphine's ceiling effect = safer take-home option

Static (prior attempt, male sex, age) are fixed and inform baseline risk. Dynamic (hopelessness, active substance use, insomnia) are what acute management actually targets. Means access — firearms, medications — is the single most actionable lever.

Symptoms in ≥2 settings, onset before age 12, >6 months, functional impairment. Methylphenidate (Addwize, Macpod) is first-line; atomoxetine (Attentrol) when stimulants aren't suitable.

Poor test effort, rapid onset linked to mood, reversible with antidepressants — unlike true dementia's consistent deficits regardless of effort or mood treatment.

Hoover's sign = a positive examination finding, not merely an absence of pathology. Symptoms are genuine and non-volitional — distinct from malingering (conscious, external gain) and factitious disorder (conscious, sick-role).

Means restriction is the most actionable suicide-risk lever Delirium = acute + fluctuating + inattention; dementia = the opposite Methylphenidate first-line for ADHD Pseudodementia reverses with antidepressants

Maslach's triad — exhaustion, depersonalisation, reduced accomplishment — is occupational, not a formal diagnosis. Major depressive disorder needs its own separate mood/anhedonia criteria. The two frequently co-occur in medical students and should be screened for independently, not collapsed into one label.

0–4 minimal · 5–9 mild · 10–14 moderate · 15–19 moderately severe · 20–27 severe. A positive item 9 (death wish) — even passive — always needs its own dedicated, structured risk assessment; the score band alone doesn't substitute for that conversation.

"We never complained" invalidation is a documented stigma barrier, independently linked to greater symptom severity and functional decline at first presentation — a measurable cost distinct from the disorder's natural course.

Hierarchy + sleep deprivation + means access + fear of disclosing to seniors converge in this population. Safety planning needs explicit means restriction and a trusted contact outside the supervisory chain.

Asking directly about distress does not plant suicidal ideation — that is a documented myth, not a real risk. Silence and "toughen up" responses delay disclosure; direct, non-judgmental questions don't cause harm and often provide relief.

Screen burnout and depression separately, not as one label Passive death wish on PHQ-9 still needs a full risk assessment Generational dismissal measurably worsens presentation severity Asking directly does not plant suicidal ideation — that's a myth

SIADH hyponatraemia: SSRI-specific elderly risk Leaden paralysis: a defining feature of atypical depression Ebstein's anomaly: the lithium-pregnancy teratogen, not neural tube defect Stevens-Johnson risk: why lamotrigine needs slow titration Hoover's sign: positive finding confirming functional neurological disorder

Active psychosis: treat now, classify duration later Wernicke's: thiamine before or with glucose, never after OCD: push SSRI dose and duration before switching class Any positive PHQ-9 item 9: structured risk assessment before discharge Peer concern: ask directly first — don't wait for explicit intent Acute EPS: anticholinergic helps; in TD, the same drug class harms