Part 1 obgyn notes Sri Lanka
    NOTES for part 1
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    🔹 ANALGESICS USED IN OBSTETRICS — LOGIC-BASED MASTER NOTE

    (PD → PK → Clinical logic → Exam locks)

    🟠 PARACETAMOL (Acetaminophen) — foundation drug

    Pharmacodynamics (WHY it works)

    • Acts centrally
    • Inhibits central COX (not peripheral)
    • Raises pain threshold + resets hypothalamic temperature set-point
    • No effect on prostaglandins in periphery → no anti-inflammatory action

    👉 Hence: analgesic + antipyretic, no gastric / platelet toxicity

    Pharmacokinetics (WHY it’s safe)

    • Oral / IV
    • Hepatic metabolism:
      • Mostly glucuronidation + sulfation
      • Small fraction → NAPQI (toxic) detoxified by glutathione
    • Half-life: 2–3 hours

    👉 Liver disease → glutathione depleted → toxicity risk

    Clinical logic

    • First-line pain control in pregnancy + postpartum
    • Safe across all trimesters
    • Combine with opioids → opioid-sparing effect

    Exam locks

    • NOT anti-inflammatory
    • Overdose → acute hepatic necrosis
    • Safe in pregnancy

    🟠 NSAIDs (Ibuprofen, Diclofenac, Indomethacin) — prostaglandin blockers

    Pharmacodynamics

    • Inhibit COX-1 & COX-2
    • ↓ prostaglandins → ↓ pain, inflammation, fever
    • ↓ prostaglandins also affect:
      • gastric mucosa
      • renal blood flow
      • uterine tone
      • fetal ductus arteriosus

    Pharmacokinetics

    • Oral
    • Hepatic metabolism
    • Short half-life (2–4 h) but physiological effects longer

    Clinical logic

    • Excellent for:
      • dysmenorrhoea
      • musculoskeletal pain
      • postpartum analgesia
    • Avoid in:
      • renal disease
      • peptic ulcer
      • aspirin-sensitive asthma

    OB logic

    • Prostaglandins maintain fetal ductus arteriosus
    • Blocking them late → ductus closure + oligohydramnios

    Exam locks

    • ❌ Avoid after 32 weeks
    • Can cause oligohydramnios
    • Indomethacin = tocolytic (short-term only)

    🔵 INDOMETHACIN (Special NSAID)

    Why it is special

    • Very potent COX inhibitor
    • Strong prostaglandin suppression

    OB relevance

    • Used as second-line tocolytic
    • GA < 32 weeks
    • Short duration (<48–72 h)

    Fetal risks (logic)

    • ↓ fetal renal perfusion → ↓ urine → oligohydramnios
    • ↓ ductal prostaglandins → ductus arteriosus constriction

    Exam locks

    • Avoid prolonged use
    • Monitor AFI if used
    • Avoid >32 weeks

    🔴 TRAMADOL — dual-mechanism weak opioid

    Pharmacodynamics

    • Weak µ-opioid agonist
    • Inhibits serotonin + noradrenaline reuptake
    • Enhances descending inhibitory pain pathways

    👉 Dual mechanism = less respiratory depression but CNS risk

    Pharmacokinetics

    • Oral / IV
    • Hepatic metabolism via CYP2D6
    • Active metabolites
    • Half-life ~ 6 hours

    Clinical logic

    • Moderate pain
    • Alternative to pethidine in labour
    • Less neonatal respiratory depression than morphine

    Risks explained

    • ↓ seizure threshold
    • ↑ serotonin → serotonin syndrome with SSRIs

    Exam locks

    • ❌ Epilepsy
    • ❌ SSRI / MAOI
    • Causes seizures at high dose

    🔴 PETHIDINE (Meperidine) — declining labour opioid

    Pharmacodynamics

    • µ-opioid agonist
    • Metabolite normeperidine = neurotoxic

    Pharmacokinetics

    • IM / IV
    • Hepatic metabolism
    • Parent half-life ~3 h
    • Metabolite half-life long → accumulation

    Clinical logic

    • Historically used in labour
    • Now avoided due to:
      • neonatal respiratory depression
      • fetal acidosis
      • maternal seizures

    Exam locks

    • Normeperidine causes seizures
    • Avoid in renal / hepatic disease
    • Avoid with MAOIs

    🔴 MORPHINE — prototype strong opioid

    Pharmacodynamics

    • Pure µ-opioid receptor agonist
    • ↓ Ca²⁺ influx presynaptic
    • ↑ K⁺ efflux postsynaptic
    • ↓ release of substance P & glutamate

    System effects (logic)

    • CNS: analgesia, sedation, euphoria
    • Respiration: ↓ CO₂ responsiveness → depression
    • GI: ↓ motility → constipation
    • CVS: histamine release → vasodilation
    • Eye: pinpoint pupils

    Pharmacokinetics

    • Poor oral bioavailability
    • Hepatic glucuronidation → M3G, M6G
    • Renal excretion → accumulation in renal failure

    OB logic

    • Crosses placenta easily
    • Neonatal respiratory depression
    • ↓ fetal heart rate variability

    Exam locks

    • Triad: coma + pinpoint pupils + respiratory depression
    • Antidote = naloxone
    • Avoid in head injury

    🟢 ENTONOX (50% N₂O + 50% O₂) — safest labour analgesic gas

    Pharmacodynamics

    • Nitrous oxide → CNS depression
    • ↑ endogenous endorphins
    • Produces analgesia without loss of consciousness

    Pharmacokinetics

    • Inhaled
    • Onset: 30–45 sec
    • Offset: 1–2 min
    • No metabolism → exhaled unchanged

    Clinical logic

    • Labour analgesia
    • Self-administered
    • Minimal maternal & fetal effects

    Exam locks

    • Contra: pneumothorax, air embolism
    • Very rapid recovery
    • Does not accumulate

    🟣 REMIFENTANIL — ultra-short acting opioid

    Pharmacodynamics

    • Potent µ-opioid agonist
    • Strong analgesia + sedation

    Pharmacokinetics (WHY it’s unique)

    • Metabolised by non-specific plasma esterases
    • Independent of liver & kidney
    • Context-insensitive half-life: 3–10 min

    👉 No accumulation even with infusion

    OB logic

    • Used as PCA in labour
    • When epidural contraindicated
    • Rapid titration + fast recovery

    Risks

    • Maternal respiratory depression
    • Neonatal respiratory depression if near delivery

    Exam locks

    • Continuous SpO₂ monitoring mandatory
    • Avoid background infusion
    • Neonatal team must be informed

    🔹 ANALGESICS USED IN OBSTETRICS — SINGLE MASTER TABLE (TRANSPOSED)

    Parameter
    Paracetamol
    NSAIDs (Ibuprofen, Diclofenac)
    Indomethacin
    Tramadol
    Pethidine (Meperidine)
    Morphine
    Remifentanil
    Entonox (50% N₂O + 50% O₂)
    Drug class / strength
    Non-opioid, mild
    Non-opioid, moderate
    Potent NSAID
    Weak opioid
    Opioid
    Strong opioid
    Ultra-short opioid
    Inhalational analgesic
    Primary mechanism (PD)
    Central COX inhibition only
    COX-1 & COX-2 inhibition
    Very strong COX inhibition
    Weak µ-agonist + ↓ 5-HT/NA reuptake
    µ-opioid agonist
    Pure µ-opioid agonist
    Potent µ-opioid agonist
    CNS depression + ↑ endorphins
    Peripheral anti-inflammatory effect
    ❌ Absent
    ✅ Present
    ✅ Strong
    ❌
    ❌
    ❌
    ❌
    ❌
    Special PD features
    Raises pain threshold; antipyretic
    ↓ PGs in stomach, kidney, uterus, ductus
    Profound PG suppression
    Dual mechanism
    Neurotoxic metabolite
    ↓ Ca²⁺ presynaptic, ↑ K⁺ postsynaptic
    Strong analgesia + sedation
    Analgesia without LOC
    Route(s)
    Oral, IV
    Oral
    Oral
    Oral, IV
    IM, IV
    Oral (poor), IV
    IV (PCA)
    Inhaled
    Metabolism
    Hepatic
    Hepatic
    Hepatic
    Hepatic (CYP2D6)
    Hepatic
    Hepatic (glucuronidation)
    Plasma esterases
    ❌ None
    Key metabolites
    NAPQI (toxic)
    —
    —
    Active metabolites
    Normeperidine (toxic)
    M3G, M6G
    Inactive
    None
    Half-life / offset
    2–3 h
    2–4 h
    Short (effect strong)
    ~6 h
    Parent ~3 h; metabolite long
    Long (↑ in renal failure)
    Context-insensitive t½ 3–10 min
    Onset 30–45 s; offset 1–2 min
    Placental transfer
    Minimal risk
    Yes
    Yes
    Yes
    Yes
    Yes (easy)
    Yes
    Minimal
    OB / clinical use
    First-line in pregnancy & postpartum
    Postpartum pain, dysmenorrhoea
    Short-term tocolysis
    Moderate pain, labour alternative
    Historical labour analgesia
    Severe pain
    Labour PCA if epidural contraindicated
    Labour analgesia
    Gestational limits
    Safe all trimesters
    ❌ Avoid >32 weeks
    ❌ Avoid >32 weeks
    Use with caution
    Avoid
    Avoid if possible
    Specialist use
    Safe
    Fetal effects (logic)
    Safe
    Ductus closure, oligohydramnios
    ↓ renal perfusion → oligohydramnios; ductal constriction
    Less neonatal depression than morphine
    Neonatal respiratory depression, acidosis
    Neonatal respiratory depression; ↓ FHR variability
    Neonatal depression if near delivery
    Minimal
    Major maternal risks
    Hepatotoxicity
    GI bleed, renal injury
    Same + fetal risks
    Seizures, serotonin syndrome
    Seizures
    Respiratory depression
    Respiratory depression
    Gas space expansion
    Key contraindications
    Severe liver disease
    PUD, renal disease, aspirin-asthma
    Prolonged use
    Epilepsy, SSRIs, MAOIs
    Renal/hepatic disease, MAOIs
    Head injury
    No background infusion
    Pneumothorax, air embolism
    Absolute exam locks
    NOT anti-inflammatory; overdose → acute hepatic necrosis
    ❌ After 32 weeks; oligohydramnios
    Tocolytic <48–72 h only; monitor AFI
    ↓ seizure threshold
    Normeperidine causes seizures
    Triad: coma + pinpoint pupils + resp depression; antidote naloxone
    Continuous SpO₂; neonatal team alert
    Rapid on/off; no accumulatio

    Morphine vs Pethidine (Meperidine)

    Domain
    Morphine
    Pethidine (Meperidine)
    Opioid class
    Strong opioid
    Synthetic opioid
    Lipid solubility
    Less lipid-soluble
    More lipid-soluble
    Onset of action
    Slower
    Faster
    Duration / Half-life
    Longer half-life
    Shorter half-life
    Placental transfer
    Crosses placenta easily
    Crosses placenta easily
    Neonatal respiratory depression
    High risk
    Lower risk (not zero)
    Primary reason for neonatal depression
    Long half-life + strong opioid effect
    Still crosses placenta but less prolonged effect
    Maternal sedation / hypnosis
    Marked ↑
    Moderate
    Maternal cooperation in labour
    Poor
    Better
    Constipation
    Present
    Less prominent
    Urinary retention
    Present
    Less
    Effect on uterine contractions
    Significant ↓
    Mild ↓
    Mechanism of uterine inhibition
    ❌ Not via oxytocin ↓ ✅ CNS depression + direct smooth muscle relaxation
    Minimal uterine smooth muscle inhibition
    Effect on labour duration
    Prolongs labour
    Less effect on labour duration
    Anticholinergic property
    Absent
    Present (mild)
    Metabolites
    No neurotoxic metabolite
    Normeperidine (neurotoxic)
    Effect on seizure threshold
    Neutral
    Lowers seizure threshold
    Use in epilepsy
    Can be used cautiously
    Contraindicated
    Repeated dosing risk
    Accumulation → respiratory depression
    Accumulation → seizures
    Typical labour use
    ❌ Avoid
    ✅ Preferred opioid
    Common combinations
    Rarely used
    Promethazine / Metoclopramide
    Overall role in labour
    Poor choice
    Drug of choice among opioids

    🧠 EXAM-LOCK MECHANISM TABLE (VERY HIGH-YIELD)

    Concept
    Morphine
    Pethidine
    Why morphine prolongs labour
    Strong CNS depression + uterine relaxation
    Minimal uterine effect
    Why neonatal depression is worse
    Long half-life
    Shorter half-life
    Why pethidine preferred
    —
    Less uterine inhibition + less neonatal depression
    Key danger
    Prolonged labour + fetal depression
    Seizures (normeperidine)

    ⚠️ CLASSIC EXAM TRAPS (DO NOT FALL)

    Statement
    Truth
    “Morphine reduces oxytocin production”
    ❌ False
    “Pethidine does not cross placenta”
    ❌ False
    “Pethidine is safe in epilepsy”
    ❌ False
    “Pethidine has no neonatal respiratory effect”
    ❌ False (just less than morphine)

    🔑 ONE-LINE EXAM ANSWER

    Pethidine is preferred over morphine in labour because it causes less uterine inhibition and less neonatal respiratory depression, despite placental transfer, while morphine significantly prolongs labour.