Brands, Medical Use, Clinical Data
- Opiate Agonists
- Capsule (sustained-release)
- Suppository (sustained-release)
- Tablet (extended-release)
Brands / Synonyms
(-)-Heroin hydrochloride; (-)-Morphine; Apokyn; Astramorph PF; Avinza; D-(-)-Morphine; Depodur; Diacetylmorphine hydrochloride; Diamorphine hydrochloride; Dulcontin; Duramorph PF; Duromorph; Embeda; Epimorph; Heroin hydrochloride; Heroine hydrochloride; Kadian; l-Morphine
; M-Eslon; M.O.S; Meconium; Morfina; Morphia; Morphin; Morphina; Morphine; Morphine Extra-Forte; Morphine Forte; Morphine H.P; Morphine Sulfate; Morphinism; Morphinum; Morphitec; Morphium; Moscontin; MS Contin; MS/L; MS/S; Msir; Nepenthe; O,O'-Diacetylmorphine hydrochloride; OMS Concentrate; Oramorph SR; Ospalivina; Rescudose; RMS Uniserts; Roxanol; Roxanol 100; Roxanol UD; Statex; Statex Drops
For the relief and treatment of severe pain.
Morphine is a narcotic pain management agent indicated for the relief of pain in patients who require opioid analgesics for more than a few days. Morphine interacts predominantly with the opioid mu-receptor. These mu-binding sites are discretely distributed in the human brain, with high densities in the posterior amygdala, hypothalamus, thalamus, nucleus caudatus, putamen, and certain cortical areas. They are also found on the terminal axons of primary afferents within laminae I and II (substantia gelatinosa) of the spinal cord and in the spinal nucleus of the trigeminal nerve. In clinical settings, morphine exerts its principal pharmacological effect on the central nervous system and gastrointestinal tract. Its primary actions of therapeutic value are analgesia and sedation. Morphine appears to increase the patient's tolerance for pain and to decrease discomfort, although the presence of the pain itself may still be recognized. In addition to analgesia, alterations in mood, euphoria and dysphoria, and drowsiness commonly occur. Opioids also produce respiratory depression by direct action on brain stem respiratory centers.
Mechanism of Action
The precise mechanism of the analgesic action of morphine is unknown. However, specific CNS opiate receptors have been identified and likely play a role in the expression of analgesic effects. The mechanism of respiratory depression involves a reduction in the responsiveness of the brain stem respiratory centers to increases in carbon dioxide tension and to electrical stimulation.
Bioavailability is approximately 30%.
LD50 = 461 mg/kg (rat, oral), 600 mg/kg (mouse, oral). Human lethal dose by ingestion is 120-250 mg of morphine sulfate. Symptoms of overdose include cold, clammy skin, flaccid muscles, fluid in the lungs, lowered blood pressure, "pinpoint" or dilated pupils, sleepiness leading to stupor and coma, slowed breathing, and slow pulse rate.
Biotrnasformation / Drug Metabolism
Primarily hepatic (90%), converted to dihydromorphinone and normorphine. Also converted to morphine-3-glucuronide (M3G) and morphine-6-glucuronide. Virtually all morphine is converted to glucuronide metabolites; only a small fraction (less than 5%) of absorbed morphine is demethylated.
ORAMORPH SR is contraindicated in patients with respiratory depression in the absence of resuscitative equipment,
in patients with acute or severe bronchial asthma and in patients with known hypersensitivity to morphine.
ORAMORPH SR is contraindicated in any patient who has or is suspected of having a paralytic ileus.
Use with Other Central Nervous System Depressants: The depressant effects of morphine are
potentiated by the presence of other CNS depressants such as alcohol, sedatives, antihistaminics, or psychotropic
drugs. Use of neuroleptics in conjunction with oral morphine may increase the risk of respiratory depression,
hypotension and profound sedation or coma.
Interaction with Mixed Agonist/Antagonist Opioid Analgesics: Agonist/antagonist analgesics (i.e.,
pentazocine, nalbuphine, butorphanol, or buprenorphine) should NOT be administered to patients who have received or
are receiving a course of therapy with a proof opioid agonist analgesic. In these patients, the mixed
agonist/antagonist may alter the analgesic effect or may precipitate withdrawal symptoms.