General Medicine
Final Professional MBBS — General Medicine. Long Questions (10 marks) and Short Notes (5 marks) across 15 systems, exam-formatted with clinical pearls, drug doses and mnemonics.
15chapters304questions48High-Yield
CLASSES OF ANTIDEPRESSANTS
Class Examples MOA Indications Key ADRs SSRIs (first-line ) Fluoxetine, Sertraline, Paroxetine, Escitalopram, Citalopram Selective serotonin reuptake inhibition → ↑ synaptic serotonin MDD (#1 indication); OCD; GAD; panic disorder; PTSD; social anxiety; bulimia GI (nausea — most common early SE; diarrhoea); sexual dysfunction (very common; ↓ libido + delayed orgasm); insomnia; headache; SIADH/hyponatraemia (especially elderly); serotonin syndrome (with MAOIs/triptans); discontinuation syndrome (especially paroxetine — FINISH ); QTc prolongation (citalopram/escitalopram) SNRIs Venlafaxine, Duloxetine, Desvenlafaxine Block serotonin + noradrenaline reuptake MDD; diabetic peripheral neuropathy (duloxetine ); GAD; fibromyalgia; stress incontinence HTN (noradrenergic — especially at high doses); nausea; sweating; discontinuation syndrome; sexual dysfunction TCAs Amitriptyline, Imipramine, Nortriptyline, Clomipramine Inhibit NA + 5-HT reuptake + anticholinergic + antihistamine + Na channel block MDD (2nd line); chronic pain (amitriptyline for neuropathic pain, migraine prophylaxis ); OCD (clomipramine ); enuresis (imipramine ) 3 C's: Cardiotoxic (↑ QRS — arrhythmia; #1 cause of death in overdose ); Convulsive; Consciousness ↓ (coma); anticholinergic (dry mouth, urinary retention, constipation, blurred vision ); postural hypotension; weight gain; LETHAL in overdose MAOIs Phenelzine, Tranylcypromine, Selegiline; Moclobemide (reversible = RIMA) Inhibit MAO-A + MAO-B → ↑ NA, 5-HT, DA Treatment-resistant depression; atypical depression (hypersomnia, hyperphagia, mood reactivity); social phobia Hypertensive crisis — 'CHEESE REACTION' (tyramine-rich foods + MAOI → unmetabolised tyramine → massive NA release → severe HTN; headache, stroke); serotonin syndrome with SSRIs/tramadol/opioids; MAOI + SSRI washout period 2 weeks (5 weeks for fluoxetine → long half-life ) Mirtazapine Mirtazapine α2-antagonist + H1 block → ↑ NA + 5-HT (NaSSA); antihistamine MDD with insomnia + poor appetite; anxiety Sedation (high antihistamine; benefit if insomnia); weight gain (H1 + 5-HT2 block → appetite ↑); agranulocytosis (rare ); minimal sexual dysfunction (advantage) Bupropion Bupropion NDRI (dopamine + noradrenaline reuptake inhibitor) MDD; smoking cessation (Zyban); ADHD Lowers seizure threshold (CI: eating disorders — bulimia/anorexia; prior seizures ); insomnia; HTN; NO sexual dysfunction (advantage); NO weight gain SEROTONIN SYNDROME
Serotonin syndrome = toxidrome from ↑↑ serotonergic activity; triad: Altered mental status (agitation, confusion) + Autonomic instability (tachycardia, HTN, hyperthermia, diaphoresis) + Neuromuscular abnormalities (tremor, hyperreflexia, clonus, myoclonus — the hallmark distinguishing from neuroleptic malignant syndrome ). Causes: MAOI + SSRI; SSRI + tramadol; linezolid + SSRI; fentanyl + SSRI. Treatment: Stop offending drug; cyproheptadine (5-HT2A antagonist); benzodiazepines (agitation); cyproheptadine 12 mg then 2 mg q2h; cooling; IV fluids.
NICOTINE DEPENDENCE
Nicotine addiction = physical + psychological dependence on nicotine in tobacco products. Fagerström test for nicotine dependence (FTND) — 6 questions; score ≥ 5/10 = significant dependence. The '5 A's' framework for brief intervention.
◆ 5 A's — Brief Smoking Cessation Intervention ▸ Ask — screen every patient for tobacco use at every visit ▸ Advise — give clear, personalised, firm advice to quit ▸ Assess — assess readiness to quit (stages of change model ) ▸ Assist — provide pharmacotherapy + behavioural counselling ▸ Arrange — arrange follow-up within 1 week of quit date WITHDRAWAL SYMPTOMS
- Onset: 4–24 hours after last cigarette; peak 2–3 days; most resolve in 2–4 weeks
- Craving (most prominent); irritability/agitation; anxiety; difficulty concentrating; increased appetite + weight gain (average 4–5 kg); insomnia; depressed mood; restlessness
- Improved health benefits timeline: 20 min — HR normalises; 24 hrs — CO eliminated; 48 hrs — smell/taste improves; 2 weeks — lung function improves; 1 year — IHD risk ↓ 50%; 5 years — stroke risk = non-smoker; 10 years — lung cancer risk ↓ 50%; 15 years — IHD risk = never-smoker
PHARMACOTHERAPY
▶ Nicotine Replacement Therapy (NRT) — patch; gum; lozenge; inhaler; nasal spray; 2× quit rate vs placebo; reduces withdrawal; start on or before quit day; combination NRT (patch + fast-acting form ) more effective than monotherapy; safe in CVD; 8–12 weeks
▶ Varenicline (Champix/Chantix) — partial agonist at α4β2 nicotinic ACh receptor; reduces craving (partial agonism) + blocks pleasure from smoking (competitive antagonism); most effective pharmacotherapy (3× quit rate vs placebo); start 1 week before quit date; 0.5 mg OD × 3 days → 0.5 mg BD × 4 days → 1 mg BD × 12 weeks ; SE: nausea (most common ), vivid dreams, depression/suicidal ideation (rare; monitor )
▶ Bupropion (Zyban) 150 mg OD × 3 days → 150 mg BD × 7–12 weeks; 2× quit rate; start 1 week before quit day; CI: seizure disorder; eating disorders
MANAGEMENT PLAN — 60-YEAR-OLD SMOKER
- Assess: FTND score; pack-years; previous quit attempts; motivation; comorbidities (COPD, IHD, cancer risk — particularly high in a 60-year-old)
- Set a quit date (within 2 weeks; commitment)
- Pharmacotherapy: Preferred — Varenicline (most effective); or NRT (patch + gum combination ); Bupropion if varenicline contraindicated
- Behavioural support: Individual or group counselling; telephone quit lines; 4 or more sessions most effective
- Anticipate withdrawal: Warn about weight gain (healthy eating; exercise); mood changes; cravings (plan alternatives)
- Monitor: Follow-up at 1 week (crisis period ); 1 month; 3 months; 1 year; CO breath test at each visit (validates abstinence)
- Relapse: Reassure; analyse triggers; modify strategy; never give up (average 8–10 attempts before sustained quit )
CLASSIFICATION
- Major Depressive Disorder (MDD) — most common; depressive episodes ± remission
- Dysthymia (Persistent Depressive Disorder) — milder but chronic (> 2 years) low mood
- Bipolar disorder — depressive + manic/hypomanic episodes
- Postnatal/Postpartum depression — within 4 weeks of childbirth; may need urgent treatment
- Seasonal Affective Disorder (SAD) — winter depression; light therapy
CLINICAL FEATURES (DSM-5)
Diagnosis: ≥ 5 symptoms for ≥ 2 weeks (must include depressed mood OR anhedonia):
◆ SIG E CAPS — DSM-5 Criteria for MDD ▸ S = Sleep disturbance (insomnia most common; hypersomnia; early morning wakening — classic — wakes 2–3 hrs before usual time) ▸ I = Interest/anhedonia (loss of pleasure; inability to feel joy; one of the 2 KEY CRITERIA ) ▸ G = Guilt/worthlessness (excessive/inappropriate) ▸ E = Energy loss/fatigue (profound; not relieved by rest) ▸ C = Concentration difficulty (forgetfulness; indecisiveness) ▸ A = Appetite change (↓ appetite + weight loss in melancholic; ↑ appetite in atypical) ▸ P = Psychomotor changes (retardation — slowed movements/speech; OR agitation) ▸ S = Suicidal ideation (always assess; passive thoughts → active plans) - Depressed mood (2nd key criterion; nearly every day; patient report or observed by others)
- Biological symptoms (melancholic features ): Early morning waking; diurnal variation (worse in morning ); marked anhedonia; psychomotor retardation/agitation; significant weight loss/anorexia
- Psychotic depression: Hallucinations or delusions (mood-congruent — guilty, nihilistic ); requires antidepressant + antipsychotic
ETIOLOGY
- Monoamine hypothesis: ↓ serotonin + noradrenaline + dopamine → depression (rationale for pharmacotherapy)
- HPA axis: Hypercortisolaemia in melancholic depression; ↑ CRH; ↓ dexamethasone suppression
- Neuroplasticity: ↓ BDNF (brain-derived neurotrophic factor); ↓ hippocampal volume; antidepressants restore neurogenesis
- Genetic: Concordance 40–60% in twins; 5-HTTLPR (serotonin transporter gene) + stressful life events interaction
- Social/Psychological: Stressful life events; childhood adversity; loss/grief; negative cognitive schema (Beck's cognitive triad: negative views of self, world, future )
TREATMENT
- Antidepressants: SSRIs first-line (sertraline 50–200 mg; fluoxetine 20–60 mg; escitalopram 10–20 mg); full response in 4–8 weeks; continue ≥ 6 months after remission (prevent relapse); lifelong if ≥ 3 recurrences
- Psychotherapy: CBT (Cognitive Behavioural Therapy ) — most evidence-based; equal efficacy to antidepressants in mild-moderate; IPT (Interpersonal Therapy ); best of all: antidepressant + CBT
- ECT (Electroconvulsive Therapy) — for severe/treatment-resistant depression ; psychotic depression; suicidal emergency (most rapid response ); postnatal depression; catatonic depression; SE: memory impairment (transient); most effective biological treatment for severe depression
- Ketamine/Esketamine (Spravato) — for treatment-resistant depression; rapid onset (hours ); IV ketamine infusion or intranasal esketamine; NMDA antagonist → rapid synaptic glutamatergic changes + BDNF ↑
OCD = psychiatric disorder characterised by obsessions (recurrent, intrusive, unwanted thoughts/images/impulses causing anxiety) AND/OR compulsions (repetitive behaviours/mental acts performed to reduce obsession-related anxiety); ego-dystonic (person recognises thoughts as own but distressing); causes significant functional impairment or > 1 hr/day.
- Common themes: Contamination (most common ) → washing compulsions; symmetry/order → arranging; harm → checking (locks, gas); religious/moral; forbidden thoughts
- Y-BOCS (Yale-Brown OC Scale) — assesses severity (obsession + compulsion subscales 0–20 each; > 8 = significant); used in clinical trials + monitoring treatment response
▶ Fluvoxamine OR Sertraline OR Fluoxetine/Paroxetine — SSRIs first-line; higher doses needed than for depression (e.g., fluoxetine 60–80 mg OD ); response in 8–12 weeks; combination SSRI + ERP (Exposure and Response Prevention — CBT) most effective
- Pathophysiology: serotonin-glutamate dysregulation in the cortico-striato-thalamo-cortical (CSTC) circuit; abnormal activity in the orbitofrontal cortex and caudate nucleus; both SSRIs (increasing serotonin) and CBT (modifying cognitive-behavioural patterns) normalise CSTC activity.
- CBT for OCD: exposure and response prevention (ERP) - the gold standard psychotherapy; the patient is exposed to the feared stimulus and prevented from performing the compulsion; repeated exposures extinguish the anxiety response.
- Differential: obsessive compulsive personality disorder (OCPD - ego-syntonic perfectionism, no true obsessions/compulsions); body dysmorphic disorder (BDD); hoarding disorder; tic disorders; autism spectrum.
▶ Clomipramine (TCA; serotonin reuptake inhibitor) — equally effective as SSRIs but worse SE; used if SSRI-resistant; augmentation with atypical antipsychotics (risperidone, aripiprazole) for SSRI-partial responders
Bipolar disorder (BD) = chronic episodic mood disorder with manic/hypomanic episodes + depressive episodes . BD-I (full mania + depression); BD-II (hypomania + depression — never full mania). Lifetime prevalence 1–2%; M = F; median onset 25 yrs.
- Classification: Bipolar I (mania + depressive episodes; mania lasts >= 7 days or requires hospitalisation); Bipolar II (hypomanic + depressive episodes; hypomania does not require hospitalisation); cyclothymia (chronic mood instability not meeting full criteria for 2+ years).
- Mania features: elevated or irritable mood, grandiosity, decreased need for sleep, pressured speech (logorrhoea), flight of ideas, distractibility, increased goal-directed activity, and risky/impulsive behaviour; psychotic features (mood-congruent grandiose delusions) in severe mania.
- Pharmacological management: acute mania - lithium, valproate, or olanzapine; haloperidol or lorazepam for agitation; maintenance - lithium (gold standard; also reduces suicide risk), valproate, lamotrigine (especially for bipolar depression); avoid antidepressant monotherapy (risk of triggering mania or rapid cycling).
- Lithium monitoring: narrow therapeutic window (0.6-1.0 mmol/L; toxic > 1.5 mmol/L); monitor levels, TFTs, and renal function every 6 months; lithium toxicity (tremor, ataxia, confusion, vomiting) is a medical emergency; treat with saline infusion and dialysis for severe toxicity.
- Mania features (DIGFAST ): D = Distractibility; I = Impulsivity/Indiscretions (spending, sex); G = Grandiosity (delusions of grandeur ); F = Flight of ideas (rapid, connected thoughts); A = Activity ↑ (goal-directed); S = Sleep ↓ (less need, not fatigued — key feature ); T = Talkative (pressured speech ). Duration ≥ 7 days (or hospitalised); significant impairment ± psychosis
▶ Acute mania: Antipsychotic (haloperidol/olanzapine/risperidone/quetiapine — rapid sedation) ± Lithium or Valproate; benzodiazepines for agitation; STOP antidepressants (can precipitate mania )
▶ Bipolar depression: Quetiapine (most evidence; FDA-approved for BD depression) OR Lurasidone; Lithium; Lamotrigine (depression prevention); AVOID antidepressant monotherapy (precipitate mania — only with mood stabiliser cover )
▶ Maintenance/mood stabilisation: Lithium (best evidence; anti-suicidal — reduces suicide in BD by 5-8×); Valproate; Lamotrigine (depression prevention); Quetiapine/Olanzapine
- Lithium monitoring: Target serum level 0.6–1.0 mEq/L (acute mania: up to 1.2 mEq/L); trough 12 hrs post-dose; check: TFT (hypothyroidism in 30%); RFT (nephrogenic DI; chronic interstitial nephritis); Ca; ECG. Toxicity (level > 1.5 mEq/L): tremor (coarse); diarrhoea; vomiting → confusion; ataxia → seizures; coma. Avoid NSAIDs + thiazides (↑ Li levels ). Pregnancy: Ebstein anomaly risk (relative risk ↑ but absolute risk low; switch to lamotrigine/valproate)
Disorder Core Feature Key Treatment Generalised Anxiety Disorder (GAD) Excessive uncontrollable worry ≥ 6 months about multiple daily life situations; somatic symptoms (muscle tension, fatigue, sleep, concentration); F > M SSRI/SNRI (escitalopram; duloxetine; venlafaxine — first-line); Buspirone (5-HT1A partial agonist; non-sedating; no dependence; slow onset 2–4 wks ); CBT; short-term benzodiazepine (avoid long-term) Panic Disorder Recurrent unexpected panic attacks (surge of intense fear; peak in 10 min; multiple somatic symptoms — palpitations, dyspnoea, chest pain, sweating, derealization ); anticipatory anxiety + agoraphobia (fear of situations where escape difficult if panic) SSRI (sertraline, escitalopram); clonazepam (short-term ); CBT (panic control therapy ); avoid benzodiazepines long-term Social Anxiety Disorder Fear of social/performance situations; most common anxiety disorder; chronic SSRI/SNRI; beta-blocker (propranolol for performance anxiety — situational use only ); CBGT (group CBT ) PTSD Trauma + hyperarousal + avoidance + intrusions (flashbacks, nightmares ); ≥ 1 month after trauma Trauma-focused CBT (first-line); EMDR; SSRI (sertraline/paroxetine FDA-approved ); prazosin (nightmares); avoid benzodiazepines Phobias Irrational fear of specific object/situation; immediate anxiety; avoidance Exposure therapy (graded exposure — gold standard); no medication for specific phobia; SSRI for social phobia - Pathophysiology: HPA axis hyperactivation with chronic cortisol elevation; amygdala hyperreactivity and reduced prefrontal cortical inhibition; serotonin, noradrenaline and GABA dysregulation.
- Treatment principles: SSRIs are first-line pharmacotherapy for all anxiety disorders (except specific phobia); SNRIs (venlafaxine) are also effective; benzodiazepines provide rapid relief but should be used short-term only (dependence risk); CBT is equally effective and has more durable benefits.
- Panic disorder: sudden intense episodes of fear with somatic symptoms (palpitations, chest pain, dyspnoea, dizziness, paraesthesia); DSM-5 requires recurrent unexpected panic attacks with anticipatory anxiety or avoidance; exclude cardiac/respiratory causes; treat with SSRI and CBT.
Schizophrenia = severe psychotic disorder; positive symptoms (delusions + hallucinations + disorganised speech + disorganised behaviour + catatonia ) + negative symptoms (Alogia, Affective blunting, Anhedonia, Avolition — 4 A's ). Onset 15–30 yrs; M = F; M earlier onset; dopamine hypothesis (mesolimbic ↑ DA + mesocortical ↓ DA ).
- Schneider first-rank symptoms: auditory hallucinations (running commentary, third-person discussions, thought echo), thought insertion/withdrawal/broadcast, passivity phenomena (made feelings, impulses, actions), and delusional perception; historically considered pathognomonic but now regarded as one cluster of features.
- Positive and negative symptoms: positive (hallucinations, delusions, disorganised thought, agitation) respond better to antipsychotics; negative (flat affect, alogia, avolition, anhedonia, social withdrawal) are more disabling, less responsive to medication, and correlate better with functional outcome.
- Antipsychotic management: typical antipsychotics (haloperidol, chlorpromazine) - D2 blockade, high EPS risk; atypical (olanzapine, risperidone, clozapine, quetiapine) - lower EPS, more metabolic side effects; clozapine - the most effective antipsychotic, reserved for treatment-resistant schizophrenia (two failed trials); requires regular monitoring for agranulocytosis (FBC weekly for first 18 weeks).
Antipsychotic Class Examples MOA Key SE Typical (1st gen) Haloperidol, Chlorpromazine, Fluphenazine, Thioridazine D2 receptor blockade in mesolimbic pathway EPS : Acute dystonia (hours — oculogyric crisis; treat: benztropine ), Akathisia (restlessness; hours–weeks; treat propranolol ), Parkinsonism (weeks; treat anticholinergics), Tardive dyskinesia (months–years; irreversible; facial involuntary movements; treat: switch to clozapine or valbenazine ); NMS (fever + rigidity + altered consciousness + autonomic instability → Dantrolene + bromocriptine ); QTc prolongation (thioridazine ) Atypical (2nd gen) Clozapine , Olanzapine, Risperidone, Quetiapine, Aripiprazole, Ziprasidone, Asenapine D2 + 5-HT2A blockade (± other receptors) ↓ EPS (less D2 blockade); Clozapine (for treatment-resistant schizophrenia — only drug proven superior for TRS ): Agranulocytosis (1%; mandatory WBC monitoring — monthly; fatal if missed); weight gain; metabolic syndrome; seizures; hypersalivation; myocarditis; sedation. Olanzapine/Quetiapine: metabolic (weight gain + DM + dyslipidaemia). Risperidone: prolactin ↑ (most among atypicals ). Aripiprazole: akathisia; less metabolic - LAI (Long-Acting Injectable) antipsychotics — depot formulations (haloperidol decanoate; paliperidone palmitate; risperidone microspheres) for non-compliance; given monthly/3-monthly; prevent relapse
Feature Delirium Dementia Onset Acute (hours to days) Insidious (months to years) Course Fluctuating (worse at night — 'sundowning' ) Slowly progressive; stable day-to-day Duration Reversible (days–weeks) Chronic; irreversible (mostly) Consciousness Impaired (altered awareness) Clear (until late stages) Attention Impaired early — cannot sustain attention Relatively preserved early; impairs later Memory Short-term impaired; some recall later Both short + long-term ; often no recall Hallucinations Visual (most common in delirium ); fleeting Less common (except DLB — Lewy body) Sleep-wake cycle Grossly disturbed Moderately disturbed Cause/Trigger Medical illness — infection, drugs, dehydration, metabolic, post-surgery Neurodegeneration: AD, VaD, DLB, FTD EEG Slow waves (metabolic slowing) Normal or mildly slow (early) Treatment Treat underlying cause ; haloperidol (hyperactive delirium ); low-dose antipsychotic; benzodiazepines (alcohol withdrawal delirium only ); melatonin AChEI (donepezil ); memantine; address CVD risk (VaD); behavioural interventions - Delirium - causes (AEIOU TIPS): Alcohol/withdrawal, Electrolytes, Infection/Inflammation, Oxygen (hypoxia), Uraemia; Trauma, Insulin (glucose), Psychiatric (rare primary cause), Structural/Stroke, drugs (the most common modifiable cause - especially anticholinergics, benzodiazepines, opioids, steroids).
- Delirium management: identify and treat the cause; non-pharmacological - reorientation, regular day-night cues, avoid restraints, familiar faces, minimise unnecessary cannulae/catheters; haloperidol 0.5-1 mg for severe agitation (not in Lewy body dementia); avoid benzodiazepines unless alcohol withdrawal.
- Dementia - types: Alzheimer disease (most common - hippocampal atrophy, amyloid plaques, tau tangles; cholinesterase inhibitors); vascular dementia (stepwise decline, cerebrovascular risk factors); Lewy body dementia (visual hallucinations, Parkinsonism, REM sleep behaviour disorder); frontotemporal dementia (personality/behaviour change, younger onset).
Feature Anorexia Nervosa (AN) Bulimia Nervosa (BN) Definition BMI < 17.5 (or < 85% ideal body weight); intense fear of gaining weight ; disturbed body image ; persistent behaviour to prevent weight gain Recurrent binge eating (rapid large amounts) + compensatory behaviours (purging — vomiting, laxatives; OR non-purging — fasting, exercise); BMI usually normal Body weight Underweight (BMI < 17.5) Usually normal or slightly overweight Key physical signs Bradycardia; hypotension; hypothermia; lanugo hair (downy body hair — starvation); amenorrhoea (key feature — hypothalamic); electrolyte imbalances; osteoporosis Parotid enlargement (from repeated vomiting); Russell's sign (calluses on dorsum of fingers from inducing vomiting ); dental erosion (acid erosion from repeated purging); hypokalaemia (from vomiting); alkalosis Most dangerous complication Hypokalaemia → cardiac arrhythmia (QTc prolongation → sudden death); refeeding syndrome (if rapid refeeding) Hypokalaemia → cardiac arrhythmia ; oesophageal rupture (Boerhaave's — rare) Treatment Weight restoration (primary goal; supervised refeeding; inpatient if BMI < 15 or haemodynamically unstable); Family-based therapy (FBT) (adolescents — Maudsley approach); CBT; olanzapine (weight gain); NO fluoxetine (not effective in underweight AN) CBT-ED (most evidence — cognitive behavioural therapy for eating disorders ); Fluoxetine 60 mg OD (FDA-approved for BN — reduces binge-purge frequency by 50%); IPT; guided self-help - Anorexia - medical complications: hypokalaemia, hyponatraemia, hypoglycaemia, anaemia; bradycardia and arrhythmias (QTc prolongation, risk of sudden death); osteoporosis; lanugo hair; amenorrhoea; refeeding syndrome on re-nutrition; multi-organ failure in severe cases.
- Bulimia - medical complications: electrolyte disturbances especially hypokalaemia (from vomiting/laxatives); Russell sign (calluses on knuckles from self-induced vomiting); dental erosion; parotid swelling; oesophageal tears; normal or slightly below-normal BMI.
- Management: multidisciplinary team; nutritional rehabilitation (managed carefully to avoid refeeding syndrome in anorexia); CBT-ED is first-line psychotherapy for both; fluoxetine (high dose 60 mg) is approved for bulimia; for anorexia, no drug has strong evidence; in-patient for BMI < 14 or rapid weight loss or medical instability.
Substance Withdrawal Onset Withdrawal Features Life-threatening? Treatment Alcohol 6–24 hrs after last drink Tremor; sweating; tachycardia; anxiety; seizures (12–48 hrs ); Delirium Tremens (48–72 hrs) YES (DT — 5–15% mortality untreated) Benzodiazepines (CIWA-Ar guided) + Thiamine Opioids Short-acting: 8–24 hrs; Long-acting: 36–48 hrs Mydriasis; piloerection; diarrhoea; yawning; myalgia; agitation; craving; anxiety No (uncomfortable but not life-threatening) Buprenorphine/naloxone; methadone; clonidine Benzodiazepines Short-acting: 1–2 days; Long-acting: 5–7 days Anxiety; insomnia; tremor; sweating; seizures ; may be life-threatening YES (similar to alcohol) Gradual taper using long-acting BZ (diazepam ); never abrupt stop Cocaine/Stimulants Hours after last use Crash: depression, fatigue, hypersomnolence, increased appetite, anhedonia (↓ DA) No Supportive; CBT; dopaminergic agents Nicotine 2–12 hrs Craving; irritability; anxiety; concentration ↓; weight gain; depressed mood No NRT; Varenicline; Bupropion - Opioid withdrawal: onset 6-24 h (short-acting) or 36-48 h (methadone); yawning, rhinorrhoea, lacrimation, piloerection, mydriasis, myalgia, diarrhoea, insomnia; not life-threatening but extremely distressing; treat with methadone, buprenorphine, lofexidine or clonidine.
- Benzodiazepine withdrawal: similar to alcohol withdrawal (both GABA modulators); can cause seizures and delirium; taper slowly over weeks; do not stop abruptly especially after long-term use.
- Nicotine withdrawal: craving, irritability, anxiety, difficulty concentrating, increased appetite, restlessness; peaks at 2-3 days; treat with varenicline, NRT or bupropion.
- Benzodiazepine withdrawal - clinical: anxiety, tremor, insomnia, and perceptual disturbances (photophobia, hyperacusis); withdrawal seizures and delirium can occur, especially after long-term high-dose use; the time course is longer than alcohol (symptoms may persist weeks to months); management is a slow structured taper.
- Cannabis withdrawal: irritability, anxiety, sleep disturbance, decreased appetite, and restlessness; onset 1-2 days after cessation; peaks day 2-6; generally self-limiting but drives relapse; no specific pharmacotherapy; CBT and motivational interviewing are helpful.
Somatoform disorders (DSM-5: Somatic Symptom and Related Disorders ) = physical symptoms not fully explained by organic disease, associated with psychological distress or impairment.
Disorder Definition Key Feature Somatic Symptom Disorder (SSD) ≥ 1 distressing somatic symptom + excessive thoughts/feelings/behaviours about the symptom Previously: Somatisation disorder; Excessive health anxiety + symptom amplification Illness Anxiety Disorder (IAD/Health Anxiety) Preoccupation with having/acquiring a serious illness; few/no somatic symptoms Reassurance-seeking; medical appointments; internet health searches Conversion Disorder (Functional Neurological Symptom Disorder) Neurological symptoms (weakness, sensory loss, seizures, blindness) inconsistent with neurological disease La belle indifférence (relative indifference to symptoms ); 'Hoover sign' (leg weakness resolves when examiner tests contralateral leg flexion ); non-epileptic attacks Factitious Disorder (Munchausen's) Deliberately produce/fake symptoms/signs in self; aware of falsification Medical records across multiple hospitals; pseudologia fantastica (elaborate lies); undergo invasive procedures Malingering Deliberate symptom production for external gain (money, avoiding work, legal benefit) Conscious motivation; stops when goal achieved; NOT a mental disorder ▶ Treatment: Therapeutic alliance (most important; empathic regular appointments); avoid unnecessary investigations; acknowledge symptoms as real; CBT (most effective overall); SSRI (for comorbid anxiety/depression ); physiotherapy (conversion disorder )
- Key DSM-5 categories: somatic symptom disorder (distressing physical symptoms + excessive health anxiety); illness anxiety disorder (fear of serious illness, minimal symptoms); conversion disorder (neurological symptoms without structural cause); factitious disorder (intentional symptom production for sick role); malingering (intentional, for external gain).
- Investigations: limited and targeted - unnecessary investigations reinforce illness behaviour and increase iatrogenic harm; explain all negative results positively; establish a single GP as the point of contact.
- Prognosis: conversion disorder has good prognosis (especially acute onset); somatic symptom disorder is chronic; all respond better to integrated care (physician + psychiatrist/psychologist).
Phenothiazines (e.g., chlorpromazine, prochlorperazine, haloperidol, fluphenazine) → D2 receptor blockade in nigrostriatal pathway → imbalance of DA/ACh → extrapyramidal side effects (EPS).
- Acute dystonia — occurs within hours to 1 week of starting/increasing antipsychotic (earliest EPS ); sustained involuntary muscle contractions:
- Oculogyric crisis (eyes deviate upward — most dramatic; pathognomonic )
- Torticollis (head/neck twisted to one side); Opisthotonus (arching of back); Trismus (jaw spasm); Laryngospasm (rare — emergency)
- Young males at highest risk; also with metoclopramide, domperidone, prochlorperazine
▶ Treatment of acute dystonia: IV/IM Benztropine 1–2 mg (anticholinergic — rapid; DOC) OR IV/IM Procyclidine 5 mg; OR Diphenhydramine 25–50 mg IV (antihistamine + anticholinergic); response in 5–15 min; continue oral anticholinergic × 2–3 days; consider dose reduction or switch to atypical antipsychotic
- Akathisia (subjective restlessness + motor agitation; 'inability to sit still' ): Propranolol 20–40 mg BD (most effective); mirtazapine; reduce antipsychotic dose; switch to quetiapine/aripiprazole
- Mechanism: dopamine D2 receptor blockade in the nigrostriatal pathway causes imbalance between dopaminergic and cholinergic systems, driving extrapyramidal symptoms; higher D2 affinity and lower atypical binding profile predict higher EPS risk (typical > atypical antipsychotics).
- EPS spectrum: acute dystonia (minutes-days), akathisia (days-weeks), Parkinsonism (weeks-months), and tardive dyskinesia (months-years); early recognition and treatment prevents complications.
- Tardive dyskinesia management: reduce or switch antipsychotic to clozapine (lowest TD risk); valbenazine or deutetrabenazine (VMAT2 inhibitors) are FDA-approved for TD; clonazepam may help; TD is often irreversible so prevention is key.
- Tardive dyskinesia (TD) — late-onset (months–years); involuntary choreiform facial movements (lip-smacking, tongue protrusion, periorbital); often irreversible; switch to clozapine; Valbenazine (FDA-approved for TD) or Deutetrabenazine
- DSM-5 Alcohol Use Disorder (AUD): ≥ 2 of 11 criteria in 12 months — impaired control, social impairment, risky use, pharmacological criteria (tolerance + withdrawal )
- CAGE questionnaire (screening): Cut down, Annoyed by criticism, Guilty, Eye-opener (morning drink ); ≥ 2 = significant AUD
Neuropsychiatric Complication Features Wernicke's encephalopathy Triad: ophthalmoplegia + ataxia + confusion; thiamine deficiency; give IV thiamine BEFORE glucose Korsakoff's psychosis Anterograde amnesia + confabulation + retrograde amnesia; chronic; irreversible; follows Wernicke's Alcoholic dementia Cognitive decline + cortical atrophy; frontal lobe; reversible with abstinence (unlike Korsakoff's) Alcoholic cerebellar degeneration Gait ataxia > limb ataxia; vermis degeneration; partial reversal with abstinence + thiamine Alcoholic peripheral neuropathy Distal sensorimotor; pain/burning; B1 + B12 deficiency; thiamine Central pontine myelinolysis Rapid correction of hyponatraemia (alcoholics are often hyponatraemic ); demyelination; locked-in syndrome - Pharmacological treatment of AUD:
- Neuropsychiatric complications in detail: Wernicke encephalopathy (ophthalmoplegia, ataxia, confusion - give IV thiamine before glucose); Korsakoff syndrome (anterograde amnesia, confabulation - chronic, largely irreversible); alcoholic cerebellar degeneration (wide-based gait, truncal ataxia, vermis predominantly); alcoholic peripheral neuropathy (distal sensorimotor, predominantly small fibre - burning dysaesthesia).
- Brief intervention: FRAMES model (Feedback, Responsibility, Advice, Menu, Empathetic, Self-efficacy); AUDIT-C questionnaire for screening; motivational interviewing for patients who are ambivalent.
- Long-term treatment goals: abstinence is ideal but harm reduction is acceptable; disulfiram (blocks ALDH, causes aversion - supervised use only); acamprosate (reduces glutamate-driven craving); naltrexone (reduces reward); community detox or in-patient depending on CIWA score and social support.
▶ Naltrexone 50 mg OD (opioid antagonist; reduces craving + reward; best evidence in AUD; injectable naltrexone monthly = Vivitrol )
Acamprosate 666 mg TDS (GABA/NMDA modulator; reduces craving; CI in renal failure )
Disulfiram (Antabuse) 200 mg OD — inhibits ALDH → acetaldehyde accumulates → aversive reaction (flushing, nausea, vomiting, palpitations); requires full abstinence; supervised administration