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CENTRAL NERVOUS SYSTEM - DETAILED NOTES (KDT & Shanbhag)

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1. GENERAL ANAESTHETICS

Classification

• Thiopentone sodium (ultra-short barbiturate)
• Propofol (most widely used)
• Etomidate
• Ketamine
• Benzodiazepines (midazolam)

Mechanism of Action (MOA)

• Inhalational agents: Enhance GABA-A receptor function (Cl⁻ channel opening) - produces CNS depression. Also inhibit NMDA receptors (especially N₂O). Meyer-Overton hypothesis - potency correlates with lipid solubility.
• Halothane: Non-explosive, hepatotoxic (halothane hepatitis via trifluoroacetyl chloride). Sensitizes myocardium to catecholamines - ventricular arrhythmias.
• N₂O (Nitrous Oxide): Called "laughing gas." Weak anaesthetic (MAC >100% - cannot produce full anaesthesia alone). Inhibits NMDA receptors. Good analgesic. Diffusion hypoxia on discontinuation (give 100% O₂ for 5-10 min). Expands gas-filled cavities - contraindicated in pneumothorax, intestinal obstruction, middle ear surgery. Can cause megaloblastic anaemia (inhibits methionine synthase - Vit B12 dependent).
• Thiopentone: Ultra short-acting because of rapid redistribution to muscle and fat (not due to metabolism). Induction dose: 5-6 mg/kg IV. No analgesic. Causes laryngospasm on stimulation. Contraindicated in porphyria.
• Propofol: "Milk of amnesia" (white emulsion). Rapid onset/offset. MOA: GABA-A receptor potentiation. Used for TIVA (total IV anaesthesia) and sedation in ICU. SE: Pain on injection, hypotension, propofol infusion syndrome (rare, fatal - metabolic acidosis, cardiac failure).

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KETAMINE (3 marks - special emphasis)

• CVS: Stimulates cardiovascular system - increases BP, HR, cardiac output (unique among anaesthetics). Due to catecholamine release. Useful in hemorrhagic shock and trauma patients.
• CNS: Increases cerebral blood flow, ICP, IOP - contraindicated in head injury, glaucoma.
• Respiratory: Bronchodilation - useful in asthmatic patients. Maintains laryngeal reflexes (unlike other GA).
• Emergence reactions: Hallucinations, vivid dreams, delirium (especially in adults). Prevented by premedication with benzodiazepines (midazolam/diazepam).

• Anaesthesia in war/field conditions (IM route), pediatric procedures, dressing of burns
• Induction in hemorrhagic shock
• Bronchospasm patients
• Short diagnostic/therapeutic procedures

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Pre-Anaesthetic Medication (PAM) - 3 marks

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2. ANTIEPILEPTIC DRUGS

Classification (Shanbhag/KDT)

1. Hydantoins: Phenytoin
2. Barbiturates: Phenobarbitone
3. Benzodiazepines: Diazepam, Clonazepam, Clobazam
4. Carboxamide: Carbamazepine, Oxcarbazepine
5. Succinimides: Ethosuximide
6. Valproate: Sodium valproate (Valproic acid)
7. Newer drugs: Lamotrigine, Gabapentin, Levetiracetam, Vigabatrin, Topiramate

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PHENYTOIN (MOA, Pharmacokinetics - Imp for exam)

• Zero-order (saturation) kinetics at therapeutic doses - small dose increase causes disproportionate rise in plasma levels
• Highly protein bound (~90%), narrow therapeutic index
• Enzyme inducer (CYP450) - drug interactions

• Dose-related: Nystagmus (earliest sign), diplopia, ataxia, mental confusion, hyperglycemia
• Chronic toxicity: Gingival hyperplasia (most common), hirsutism, coarsening of facial features, megaloblastic anaemia (folate deficiency), peripheral neuropathy, osteomalacia
• Teratogenicity: "Fetal Hydantoin Syndrome" - cleft palate, cardiac defects, microcephaly

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CARBAMAZEPINE

• Diplopia, ataxia, drowsiness (most common)
• SIADH (syndrome of inappropriate ADH) - hyponatremia - important SE
• Blood dyscrasias: Aplastic anaemia, agranulocytosis (rare but serious) - CBC monitoring needed
• Teratogenicity: Neural tube defects (spina bifida)
• SJS (Stevens-Johnson syndrome)
• Enzyme inducer - reduces efficacy of OCP, warfarin

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VALPROATE (Sodium Valproate)

1. Blocks Na⁺ channels
2. Blocks T-type Ca²⁺ channels (important for absence seizures)
3. Increases GABA by inhibiting GABA transaminase (GABA-T) and succinic semialdehyde dehydrogenase
4. Blocks NMDA receptors

• Hepatotoxicity (most serious, potentially fatal - especially in children <2 years)
• Teratogenicity: Neural tube defects (spina bifida) - most teratogenic AED
• Weight gain, hair loss (alopecia), tremor, GI upset
• Pancreatitis (rare)
• Thrombocytopenia

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NEWER ANTIEPILEPTICS

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STATUS EPILEPTICUS - Treatment (5 marks)

• Lorazepam IV 0.1 mg/kg (DOC if available) OR
• Diazepam IV 0.1-0.2 mg/kg (followed by phenytoin to prevent recurrence) OR
• Midazolam IM (if no IV access)

• Phenytoin IV 20 mg/kg (in NS, max 50 mg/min)
• Or Fosphenytoin 20 mg PE/kg
• Valproate IV (alternative)

• Phenobarbitone IV 20 mg/kg
• Propofol infusion
• Thiopentone anaesthesia with mechanical ventilation

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3. OPIOID ANALGESICS

Classification

• Morphine (prototype)
• Codeine (methylmorphine)
• Papaverine (no analgesic, antispasmodic)
• Thebaine (precursor for synthesis)

• Heroin (diacetylmorphine, most potent, most addicting)
• Hydromorphone
• Oxycodone
• Buprenorphine

• Pethidine (Meperidine) - DOC for biliary/renal colic (causes less spasm of Oddi's sphincter; but actually increases it - not spasmogenic as morphine), obstetric analgesia
• Tramadol - Weak opioid + inhibits NA/5-HT reuptake; least abuse potential
• Fentanyl - 80-100x more potent than morphine; used in patches for chronic pain, epidural
• Methadone - Long-acting; used in opioid detoxification programs
• Sufentanil - Most potent synthetic opioid (500-1000x morphine)

• Buprenorphine: Partial agonist at μ (mu), antagonist at κ (kappa). High affinity, slow dissociation from μ - ceiling effect. Used in opioid dependence treatment (OPIOID SUBSTITUTION THERAPY). Sublingual administration. Naloxone partially reverses it.
• Pentazocine: Agonist at κ, partial agonist/antagonist at μ. Analgesic but can precipitate withdrawal in opioid-dependent patients. Can raise BP and HR (unlike morphine). Causes dysphoria.
• Nalbuphine: κ agonist, μ antagonist.
• Butorphanol: κ agonist, μ partial agonist.

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MORPHINE - Detailed Pharmacology

• μ (mu/OP3): Supraspinal analgesia, euphoria, respiratory depression, physical dependence, decreased GI motility
• κ (kappa/OP2): Spinal analgesia, sedation, miosis, dysphoria
• δ (delta/OP1): Spinal analgesia, modulates μ activity

• Analgesia - acts at dorsal horn, PAG (periaqueductal gray), limbic system
• Euphoria - activates mesolimbic dopamine pathway
• Sedation/drowsiness
• Miosis (pupillary constriction) - stimulates Edinger-Westphal nucleus (oculomotor nerve). Pathognomonic sign of opioid toxicity (pin-point pupils). No tolerance develops to miosis.
• Respiratory depression - reduced sensitivity of respiratory center to CO₂ (most dangerous). Tolerance develops.
• Antitussive - Codeine > Morphine. Suppresses cough center in medulla.
• Nausea/vomiting - stimulates CTZ (chemoreceptor trigger zone)

• Decreases peristalsis, increases tone of smooth muscle - CONSTIPATION (no tolerance develops)
• Increases tone of sphincter of Oddi - raises intrabiliary pressure (avoid in biliary colic - use pethidine instead)
• Urinary retention (increases urethral sphincter tone)

• Poor oral bioavailability (high first-pass)
• Crosses placenta - neonatal respiratory depression
• Active metabolite: Morphine-6-glucuronide (M6G) - more potent analgesic
• Excreted in urine (dose adjustment in renal failure)

1. Coma
2. Respiratory depression (slow, shallow breathing)
3. Pin-point pupils (miosis)

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NALOXONE (3 marks)

• Reverses all effects of opioids within 1-2 minutes IV
• Short duration (~30-60 min) - may need repeated dosing
• Precipitates acute withdrawal in opioid-dependent patients
• No agonist activity - gives no analgesia alone
• IV/IM/SC/intranasal routes
• Dose: 0.4-2 mg IV; repeat every 2-3 min as needed
• Also used in diagnosis of opioid dependence (naloxone challenge test)

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4. ANTI-PARKINSONIAN DRUGS

Classification

1. Dopamine precursor: Levodopa (with peripheral decarboxylase inhibitor)
2. Dopamine agonists: Bromocriptine, Pramipexole, Ropinirole, Cabergoline, Rotigotine (patch)
3. MAO-B inhibitors: Selegiline, Rasagiline
4. COMT inhibitors: Entacapone, Tolcapone
5. Releasing agents: Amantadine
6. Inhibitors of DA reuptake: Amantadine

• Trihexyphenidyl (Benzhexol), Procyclidine, Biperiden
• Useful mainly for tremor

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LEVODOPA (DOC for Parkinson's) - Detailed

• Levodopa is rapidly converted to dopamine peripherally by DOPA decarboxylase - causing nausea, vomiting, hypotension, cardiac arrhythmias
• PDDIs (Carbidopa, Benserazide) do NOT cross BBB - they inhibit peripheral (but not central) decarboxylation
• This reduces peripheral SE, increases levodopa reaching brain, allows 75% dose reduction of levodopa
• Carbidopa + Levodopa = Syndopa, Sinemet
• Benserazide + Levodopa = Madopar

• Improves bradykinesia and rigidity most dramatically
• Tremor less responsive
• Akinesia, gait disturbance improve

• Peripheral: Nausea/vomiting (CTZ stimulation), postural hypotension, cardiac arrhythmias
• Central (long-term - dyskinesias):
  • "On-Off" phenomenon: Abrupt fluctuations between mobility (on) and immobility/rigidity (off)
  • End-of-dose wearing off (short-duration response)
  • Peak-dose dyskinesias: Involuntary choreoathetoid movements
  • Psychiatric: Hallucinations, psychosis, vivid dreams
• "Cheese effect" - Levodopa is tyramine precursor - take with MAO-B inhibitor carefully

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PERIPHERAL DECARBOXYLASE INHIBITORS (PDDIs) - 3 marks

• Carbidopa and Benserazide
• Do not cross BBB
• Inhibit DOPA decarboxylase peripherally
• Reduce peripheral conversion of L-DOPA to dopamine
• Benefits: Reduce dose of levodopa by 75%, reduce peripheral SE (nausea, vomiting, hypotension, arrhythmias)
• Do NOT inhibit central conversion (do not reduce efficacy)
• Never used alone (no anti-parkinson effect alone)

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SELEGILINE (MAO-B Inhibitor) - 3 marks

• Irreversible, selective MAO-B inhibitor
• MAO-B preferentially metabolizes dopamine in the striatum
• Reduces breakdown of dopamine - prolongs its action
• Also prevents formation of neurotoxic MPTP metabolite (MPP+) - possible neuroprotective role
• Used as adjuvant with levodopa - reduces "wearing off" effects
• At high doses may inhibit MAO-A - hypertensive crisis with tyramine-rich food ("cheese effect")
• SE: Insomnia (amphetamine metabolites), hypertension in high doses

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COMT INHIBITORS - 3 marks

• Entacapone (peripheral only) and Tolcapone (central + peripheral)
• COMT (Catechol-O-Methyl Transferase) metabolizes levodopa and dopamine
• Inhibiting COMT prolongs the action of levodopa and dopamine
• Used as adjuvant to levodopa to treat "wearing off" effects
• Tolcapone: Hepatotoxic (liver monitoring needed)

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5. SEDATIVE-HYPNOTICS

Classification

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BENZODIAZEPINES - Detailed (5 marks)

• GABA opens Cl⁻ channel → hyperpolarization → CNS depression
• BZDs increase the FREQUENCY of Cl⁻ channel opening (allosteric modulation - require GABA to be present; cannot work alone unlike barbiturates)
• Barbiturates increase DURATION of Cl⁻ channel opening

• Ultra-short acting (t½ <6h): Triazolam, Midazolam
• Short-acting (t½ 6-24h): Lorazepam, Oxazepam, Alprazolam
• Long-acting (t½ >24h): Diazepam, Nitrazepam, Flurazepam, Chlordiazepoxide, Clonazepam

• Anxiolysis, sedation, hypnosis
• Muscle relaxation (enhance spinal cord GABA - reduce polysynaptic reflexes)
• Anticonvulsant (Diazepam, Clonazepam, Lorazepam)
• Anterograde amnesia (no retrograde amnesia)
• Minimal respiratory/cardiovascular depression (advantage over barbiturates)

• Anxiety disorders (GAD, panic disorder)
• Insomnia (short-term use only)
• Status epilepticus (diazepam/lorazepam IV)
• Muscle spasm (diazepam)
• Alcohol withdrawal (chlordiazepoxide, diazepam - long-acting preferred)
• Premedication for surgery
• Procedural sedation (midazolam)

• Tolerance develops to hypnotic/anxiolytic effect
• Physical and psychological dependence - withdrawal syndrome (anxiety, tremors, seizures)
• Rebound insomnia on stopping
• Daytime drowsiness, cognitive impairment, falls in elderly
• Paradoxical reactions (rage, aggression) in some patients

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BARBITURATES

• CNS depression dose-dependent - from sedation → hypnosis → anaesthesia → coma → death
• Respiratory depression (very dangerous - no ceiling effect)
• Enzyme induction (CYP450) - many drug interactions
• Tolerance and severe physical dependence - dangerous withdrawal (life-threatening seizures)
• No specific antagonist (unlike BZDs - flumazenil)
• Precipitate acute porphyria
• No analgesic effect (may be antianalgesic at low doses)

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NON-BZD HYPNOTICS (Z-drugs) - 5 marks

• Zolpidem, Zaleplon, Eszopiclone (Zopiclone)
• Act on BZD (omega-1) receptor subtype selectively (α1 subunit of GABA-A) - selective hypnotics
• Less anxiolytic, muscle relaxant, and anticonvulsant effects compared to BZDs
• Shorter half-life, less residual daytime sedation
• Less dependence/tolerance than barbiturates, slightly less than BZDs
• Zaleplon: shortest t½ (1h) - can be taken in middle of night

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6. ANTIPSYCHOTIC DRUGS

Classification

• Phenothiazines: Chlorpromazine, Thioridazine, Fluphenazine, Trifluoperazine
• Butyrophenones: Haloperidol (most widely used typical), Droperidol
• Thioxanthenes: Flupenthixol, Zuclopenthixol

• Clozapine (prototype atypical - D4 blocker, no EPS, causes agranulocytosis)
• Risperidone, Olanzapine, Quetiapine, Ziprasidone, Aripiprazole (partial D2 agonist), Amisulpride

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CHLORPROMAZINE (Prototype) - Detailed

1. Acute dystonia (hours-days): Oculogyric crisis, torticollis, tongue protrusion. Tx: Anticholinergics (benztropine, trihexyphenidyl)
2. Akathisia (days-weeks): Motor restlessness, inability to sit still. Tx: Propranolol, BZDs
3. Parkinsonism (weeks-months): Drug-induced Parkinsonism - bradykinesia, rigidity, tremor. Tx: Anticholinergics or dose reduction
4. Tardive Dyskinesia (months-years): Repetitive, involuntary movements (especially orofacial). Irreversible if not caught early. Worsened by anticholinergics. Tx: Clonazepam, Valbenazine, reduce dose.

• Sedation (H1 block)
• Postural hypotension (α1 block)
• Anticholinergic: dry mouth, blurred vision, urinary retention, constipation
• Hyperprolactinemia: Galactorrhea, amenorrhea, gynecomastia, sexual dysfunction
• NMS (Neuroleptic Malignant Syndrome): Life-threatening. Hyperthermia, rigidity, altered consciousness, autonomic instability. Tx: Stop drug, Dantrolene + Bromocriptine
• Lowering seizure threshold
• Photosensitivity, QTc prolongation (especially thioridazine - withdrawn)
• Agranulocytosis (especially clozapine - weekly WBC monitoring)

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7. ANTI-DEPRESSANTS: TCA, SSRI, SNRIs

Tricyclic Antidepressants (TCA) - 5 marks (includes "Acute ethanol overdose + chronic alcoholism")

• Depression (all subtypes)
• Enuresis (bedwetting): Imipramine - DOC for childhood nocturnal enuresis
• Panic disorder, OCD (Clomipramine)
• Neuropathic pain (amitriptyline)
• Migraine prophylaxis

• Anticholinergic toxidrome: Dry mouth, tachycardia, hyperthermia, urinary retention, mydriasis, delirium - "Dry as a bone, Red as a beet, Hot as a hare, Mad as a hatter"
• Cardiotoxicity (most dangerous): Prolonged QRS and QT, wide-complex tachycardia, ventricular arrhythmias, hypotension. Due to Na⁺ channel blockade. Tx: IV Sodium Bicarbonate (alkalinizes plasma - reduces protein binding of TCA, and increases Na⁺)
• Seizures (lower seizure threshold)
• Coma

• Methanol → Formaldehyde → Formic acid (toxic metabolite - causes metabolic acidosis + retinal toxicity → blindness)
• Tx: Ethanol (competitive inhibitor of alcohol dehydrogenase) or Fomepizole (4-MP - inhibitor of ADH) + sodium bicarbonate + folic acid + hemodialysis
• Chronic alcoholism: Disulfiram (antabuse reaction), Naltrexone, Acamprosate for treatment

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SSRI (Selective Serotonin Reuptake Inhibitors) - 5 marks

• Depression (first-line with SNRIs)
• OCD (Fluvoxamine, Fluoxetine, Paroxetine)
• Panic disorder, Social phobia, PTSD, GAD
• Bulimia nervosa (Fluoxetine)
• PMDD (premenstrual dysphoric disorder)

• Sexual dysfunction (most common: delayed ejaculation, anorgasmia) - most common reason for discontinuation
• Nausea/GI upset (early, usually settles)
• Insomnia or sedation
• Serotonin Syndrome (with other serotonergic drugs or MAOIs): Hyperthermia, agitation, tremor, clonus, diarrhea, diaphoresis. Tx: Cyproheptadine (5-HT antagonist), BZDs.
• Hyponatremia (SIADH)
• Bleeding risk (reduce platelet aggregation)

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8. LITHIUM - 5 marks

• Inhibits inositol monophosphatase - depletes inositol for second messenger (IP3 system) - "Inositol depletion theory"
• Inhibits glycogen synthase kinase-3β (GSK-3β)
• Modulates Na⁺/K⁺ ATPase
• Reduces DA and NA neurotransmission; increases serotonin

• DOC for Bipolar Disorder (Manic-depressive illness): Both acute mania treatment and long-term prophylaxis
• Prophylaxis of recurrent unipolar depression
• Cluster headache
• Augmentation of antidepressants in treatment-resistant depression
• Neutropenia (increases WBC)

• Lethargy, tremor (fine tremor - earliest SE, treated with propranolol), ataxia
• Increase in urine (Nephrogenic DI - blocks ADH at collecting duct)
• Thyroid: Hypothyroidism, goiter (blocks iodine uptake)
• Heart: ECG changes (T-wave flattening/inversion - usually benign)
• Interaction with NSAIDs, thiazides (increase lithium levels - toxicity)
• Upset stomach, weight gain, acne
• Memory impairment, cognitive effects

• Coarse tremor, ataxia, confusion, seizures, coma
• Tx: Stop drug, hydration with normal saline, hemodialysis in severe cases

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9. SKELETAL MUSCLE RELAXANTS

Classification

• Short: Mivacurium
• Intermediate: Atracurium, Vecuronium, Rocuronium, Cisatracurium
• Long: Pancuronium, Tubocurarine (prototype, d-TC)

• Succinylcholine (Suxamethonium) - only one in clinical use

• Diazepam, Baclofen (GABA-B agonist), Tizanidine (α2 agonist), Mephenesin, Chlorzoxazone, Carisoprodol, Methocarbamol

• Dantrolene (blocks Ca²⁺ release from SR)

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SUCCINYLCHOLINE (Suxamethonium) - 5 marks (Shanbhag emphasis)

• Fastest onset (60-90 sec) and shortest duration (5-10 min) of all NMBs
• DOC for rapid sequence intubation (RSI) - emergency intubation
• Used with succinylcholine phase I (depolarizing) → phase II (desensitization) block with repeated doses

• Hyperkalemia: K⁺ efflux from muscle during depolarization - dangerous (↑ 0.5-1 mEq/L normally). Contraindicated in burns, crush injury, denervation injuries, upper motor neuron lesions (massive K⁺ release → cardiac arrest)
• Malignant Hyperthermia (MH): Rare pharmacogenetic disorder (RYR1 mutation). Massive Ca²⁺ release from SR → uncontrolled muscle contraction, hyperthermia, metabolic acidosis. Tx: Dantrolene (DOC) + cooling + NaHCO₃
• Prolonged apnea: In patients with pseudocholinesterase deficiency (dibucaine number low - <20%)
• Muscle pain (post-succinylcholine myalgia)
• Bradycardia (especially with repeated doses)
• Increased IOP, ICP, intragastric pressure

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COMPETITIVE (Non-depolarizing) NMBs

• Atracurium: Undergoes Hofmann elimination (spontaneous pH and temperature-dependent degradation) - safe in hepatic and renal failure. Histamine release (hypotension). Metabolite laudanosine (CNS excitatory - seizures in high doses).
• Vecuronium: No CV effects, no histamine release; steroid-based.
• Rocuronium: Fastest onset among non-depolarizing blockers; reversed by Sugammadex.
• Pancuronium: Vagolytic (increases HR); long acting.

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DANTROLENE - 3 marks

• Malignant Hyperthermia (DOC) - IV dantrolene 2.5 mg/kg
• NMS (Neuroleptic Malignant Syndrome) - adjuvant to bromocriptine
• Spasticity in upper motor neuron disorders (MS, cerebral palsy, spinal cord injury) - oral

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10. LOCAL ANAESTHETICS (LA)

Classification

• Cocaine (prototype; also causes vasoconstriction - used in nasal surgery)
• Procaine (PABA derivative; low toxicity; used in penicillin depot preparations)
• Benzocaine (topical only; used for mucous membranes)
• Tetracaine (amethocaine) - most potent ester; used in spinal anaesthesia

• Lidocaine (lignocaine) - prototype amide; also class IB antiarrhythmic
• Bupivacaine - most cardiotoxic; most commonly used for spinal anaesthesia; longest acting
• Ropivacaine - less cardiotoxic than bupivacaine; useful in epidurals (spares motor fibers)
• Prilocaine - causes methemoglobinemia
• Mepivacaine, Levobupivacaine

• Esters: Hydrolyzed by plasma cholinesterase (pseudocholinesterase); produce PABA → allergic reactions more common
• Amides: Metabolized in liver by CYP450; less allergic reactions; longer acting

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MOA of Local Anaesthetics

• Blocks voltage-gated Na⁺ channels on nerve membrane - prevents depolarization
• Enter the nerve in uncharged (base) form, then re-ionize inside the cell (acidic intracellular)
• Charged (cation) form blocks Na⁺ channel from inside
• "Use-dependent block" - more effective in rapidly firing nerves
• Order of fiber block: Small C fibers (pain, temperature) first, then small myelinated fibers, then large fibers (motor, touch, pressure) last
• Inflammation reduces efficacy of LAs (acidic environment in infected tissue - more drug in ionized form, cannot penetrate membrane)

• Causes vasoconstriction - reduces systemic absorption, prolongs duration of action, reduces toxicity
• Contraindicated in end-artery areas (digits, penis, nose, ears, ring block) - ischemia/necrosis
• CI in IV regional anaesthesia (Bier's block)

• CNS: (low plasma levels) perioral tingling, lightheadedness, tinnitus → (higher) visual disturbances, convulsions → (very high) CNS depression, coma
• CVS: Bupivacaine - most cardiotoxic - reentrant arrhythmias; Na⁺ channel block in cardiac muscle
• Tx of LA toxicity: Stop injection, O₂, IV lipid emulsion (20% Intralipid) is DOC for severe cardiotoxicity - "lipid sink" theory

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TECHNIQUES OF LA

1. Topical/Surface anaesthesia: Cocaine, Lignocaine, Benzocaine
2. Infiltration anaesthesia: Procaine, Lignocaine
3. Nerve block: Lignocaine, Bupivacaine (major nerve blocks, dental)
4. IV regional anaesthesia (Bier's block): Lignocaine only (NO epinephrine)
5. Epidural (extradural): Bupivacaine, Ropivacaine, Lignocaine; used in labour analgesia
6. Spinal (intrathecal/subarachnoid): Bupivacaine (heavy/isobaric), Tetracaine, Lignocaine
7. Caudal block: Bupivacaine, Lignocaine (via sacral hiatus)

• Hypotension (sympathetic block - give IV fluids, vasopressors)
• Post-dural puncture headache (PDPH) - treat with bed rest, hydration, caffeine; blood patch if persistent
• Urinary retention, spinal hematoma, total spinal block (rare)

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QUICK REFERENCE SUMMARY TABLE

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Reference: Based on Katzung's Basic & Clinical Pharmacology 16th Ed (KDT) and Shanbhag's Review of Pharmacology. Page numbers in your notes correspond to Tripati/Shanbhag editions.