Opioids Flashcards
(17 cards)
Morphine – therapeutic uses and important adverse effects
Principal clinical uses
- Potent analgesic for severe acute pain (trauma, postoperative, burns, renal & biliary colic, cancer, visceral & ischaemic pain)
- Acute left‑ventricular failure & pulmonary oedema – venodilates, relieves ‘air‑hunger’
- Myocardial infarction to allay pain, anxiety & sympathetic drive
- Premedication & spinal/epidural analgesia; relief of obstetric pain (cautiously).
Key adverse drug reactions (dose‑related unless stated)
- Sedation, mental clouding, euphoria/dysphoria
- Respiratory depression – major dose‑limiting toxicity
- Miosis, nausea‑vomiting (CTZ), marked constipation & biliary spasm
- Histamine release → hypotension, pruritus, bronchoconstriction—dangerous in asthmatics
- Urinary retention (esp. elderly men), bradycardia; tolerance & physical dependence on repeated use
Pentazocine – pharmacological profile, uses, cautions
- First κ‑agonist / weak μ‑antagonist ‘mixed’ opioid; analgesic ceiling lower than morphine; mostly spinal action .
- Produces 1/3–½ morphine’s sedation & respiratory depression with a ceiling effect; constipation & biliary spasm milder .
- Sympathomimetic: tachycardia & ↑BP at higher doses—avoid in coronary ischaemia/MI .
- Dysphoria & psychotomimetic effects at >60 mg due to σ‑receptor activity; abuse potential low, can precipitate withdrawal in μ‑dependent patients .
- Orally effective (50–100 mg) or IM/SC (30–60 mg) every 3‑5 h; used only for moderate postoperative, burn/trauma or cancer pain when full agonists undesirable .
Buprenorphine – key features, clinical usefulness & cautions
- Highly lipid‑soluble thebaine congener; partial μ‑agonist & κ‑antagonist, ~25 × morphine potency but with low intrinsic activity and ceiling effect on analgesia & respiratory depression .
- Slow onset, long duration (analgesia 6–8 h; accumulates on repeat dosing → ~24 h) .
- ADR: sedation, vomiting, miosis like morphine but less constipation; prominent postural hypotension; difficult to reverse with naloxone; can precipitate withdrawal in high‑level μ‑dependence .
- Sublingual (0.2–0.4 mg q6‑8 h) or IM/SC 0.3 mg; indicated for long‑lasting pain (cancer), MI analgesia, peri‑operative pain and as an alternative to methadone in opioid‑dependence programmes .
- Not recommended during labour—neonatal respiratory depression poorly reversed by naloxone .
Pethidine (Meperidine) – distinguishing properties, uses & hazards
- Synthetic μ‑agonist, analgesic potency ≈1/10 morphine but similar efficacy; faster onset, shorter action (2–4 h) .
- Anticholinergic structure → tachycardia, dry mouth, less miosis/constipation; weaker spasmogenic effect so preferred for biliary & renal colic; less histamine release—safer in asthma, used for labour analgesia & as pre‑anaesthetic .
- Nor‑pethidine metabolite (after repeated/large doses or in renal failure) causes CNS excitation, tremors, seizures—limit use .
- Interacts dangerously with MAOIs (excitatory) and SSRIs (serotonin syndrome).
- Dose 50–100 mg IM/SC; occasional IV for shivering. Declining role due to toxicity profile .
Tramadol – mechanism, therapeutic role & adverse effects
- ‘Atypical’ centrally acting analgesic: weak μ‑agonist plus inhibitor of noradrenaline & 5‑HT re‑uptake → augments descending monoaminergic pain pathways; analgesia only partly naloxone‑reversible .
- Equi‑analgesic: IV 100 mg ≈ IM 10 mg morphine; oral bioavailability good; t½ 5–6 h, duration 4–6 h .
- Minimal respiratory depression, constipation or haemodynamic change—safe in cardiovascular disease; but causes nausea, dizziness, sweating; lowers seizure threshold and can precipitate serotonin syndrome with SSRIs .
- Indicated for moderate acute postoperative/trauma pain and chronic musculoskeletal or cancer pain where NSAIDs inadequate; usual dose 50–100 mg PO/IM/slow IV q4–6 h .
Why is morphine useful in acute left-ventricular failure?
Morphine acts as a venodilator reducing preload, mildly reduces afterload via arteriolar dilation, relieves anxiety, and depresses the respiratory centre—collectively reducing pulmonary congestion and alleviating ‘air hunger’.
Why is morphine contraindicated in head injury?
Morphine-induced respiratory depression leads to CO₂ retention, causing cerebral vasodilation and increased intracranial pressure. Additionally, miosis masks neurologic signs, and vomiting increases aspiration risk.
Why is naloxone the drug of choice in opioid poisoning?
Naloxone is a pure competitive antagonist at μ, κ, and δ opioid receptors. It quickly reverses CNS and respiratory depression caused by opioids without any intrinsic agonist activity.
Why should pentazocine be avoided in cardiac disease?
Pentazocine has sympathomimetic properties, increasing heart rate and blood pressure. This raises myocardial oxygen demand, potentially precipitating angina or arrhythmias.
Why is buprenorphine not recommended for obstetric labour pain?
Its long half-life and strong receptor binding can cause prolonged neonatal respiratory depression, which is difficult to reverse with naloxone due to buprenorphine’s high affinity.
Why is methadone used as substitution therapy in opioid dependence?
Methadone is orally effective with a long half-life (24–36 h), producing stable plasma levels and minimal euphoria. It prevents withdrawal symptoms and allows controlled tapering.
Why is pethidine preferred over morphine in biliary colic?
Pethidine causes less spasm of the sphincter of Oddi than morphine, providing better pain relief with less increase in biliary tract pressure.
Why is naltrexone used in most de-addiction centres?
Naltrexone is a long-acting oral opioid antagonist that blocks the euphoric effect of opioids. It has no abuse potential and can be given three times weekly.
Explain: Morphine helps in cardiac asthma but is contraindicated in bronchial asthma.
In cardiac asthma (pulmonary oedema), morphine reduces preload and anxiety, relieving symptoms. In bronchial asthma, it may worsen bronchospasm via histamine release and cause dangerous respiratory depression.
Why can opioids be used in diarrhoea?
Opioids act on enteric μ-receptors to reduce propulsive motility and increase segmenting contractions, prolonging transit time and allowing more water absorption—useful in controlling non-infective diarrhoea.
Role of methadone and naltrexone in morphine de-addiction programmes
Methadone is used for maintenance and tapering due to its long-acting agonist properties. After detoxification, naltrexone is given to block the euphoric effect of any relapsed opioid and prevent abuse.
Classify opioids, give key uses and contraindications.
Classification:
- Natural: Morphine, Codeine
- Semi-synthetic: Heroin, Oxycodone, Buprenorphine
- Synthetic: Pethidine, Methadone, Fentanyl, Tramadol
- Receptor-based: Full agonists (morphine, fentanyl), partial agonist (buprenorphine), mixed (pentazocine), antagonists (naloxone, naltrexone)
Key therapeutic uses:
- Severe pain: Morphine
- MI pain: Morphine
- Cancer pain: Fentanyl patch, SR morphine
- Obstetric labour: Pethidine
- Balanced anaesthesia: Fentanyl
- Cough: Codeine
- Diarrhoea: Loperamide
- De-addiction: Methadone, Naltrexone
Contraindications:
- Head injury (↑ICP)
- Bronchial asthma/COPD (bronchospasm)
- Acute abdomen (masks diagnosis)
- Liver/renal failure (drug accumulation)
- Pregnancy near term (neonatal depression)
- MAOI use (with pethidine, tramadol – serotonin syndrome)
