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Active ingredient: Hydromorphone - Brands, Medical Use, Clinical Data

Brands, Medical Use, Clinical Data

Drug Category

  • Analgesics, Opioid
  • Narcotics

Dosage Forms

  • Capsule (controlled-delivery)
  • Solution
  • Tablet

Brands / Synonyms

Dihydromorfinon; Dihydromorfinon [Czech]; Dihydromorphinone; Dilaudid; Dilaudid Oros; Dilaudid-HP; DiMo; Dimorphone; Hidromorfona [INN-Spanish]; Hydromorfona [Spanish]; Hydromorphon; Hydromorphone; Hydromorphone HCL; Hydromorphonum [INN-Latin]; Hymorphan; Idromorfone; Idromorfone [DCIT]; Laudacon; Laudicon; Morphinone, dihydro-; Novolaudon; Palladone; Paramorphan

Indications

For the relief of moderate to severe pain such as that due to surgery, cancer, trauma/injury, burns, myocardial infarction and colic.

Pharmacology

Hydromorphone is a hydrogenated ketone derivative of morphine that acts as a narcotic analgesic. It has a shorter duration of action than morphine. Hydromorphone is approximately 8 times more potent on a milligram basis than morphine. In addition, hydromorphone is better absorbed orally than is morphine. In clinical settings, Hydromorphone exerts its principal pharmacological effect on the central nervous system and gastrointestinal tract. Its primary actions of therapeutic value are analgesia and sedation. Hydromorphone 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

Hydromorphone is a narcotic analgesic; its principal therapeutic effect is relief of pain. Hydromorphone interacts predominantly with the opioid mu-receptors. 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, Hydromorphone exerts its principal pharmacological effect on the central nervous system and gastrointestinal tract. Hydromorphone also binds with kappa-receptors which are thought to mediate spinal analgesia, miosis and sedation.

Absorption

Better absorbed orally than morphine

Toxicity

Hydromorphone is a schedule II narcotic which can lead to physical dependence or addiction. High doses lead to respiratory depression, nausea, and vomiting. Overdoses lead to extreme somnolence progressing to stupor or coma, skeletal muscle flaccidity, cold and clammy skin, and sometimes bradycardia and hypotension. In severe overdosage, apnea, circulatory collapse, cardiac arrest and death may occur.

Biotrnasformation / Drug Metabolism

Primarily hepatic. After absorption hydromorphone is metabolized by the liver to the glucuronide conjugate which is then excreted in the urine. Hydromorphone is metabolized to the major metabolites hydromorphone-3-glucuronide, hydromorphone-3-glucoside and dihydroisomorphine-6-glucuronide.

Contraindications

DILAUDID is contraindicated in patients with a known hypersensitivity to hydromorphone; in the presence of an intracranial lesion associated with increased intracranial pressure; and whenever ventilatory function is depressed (chronic obstructive pulmonary disease, cor pulmonale, emphysema, kyphoscoliosis, status asthmaticus).

Drug Interactions

Patients receiving other narcotic analgesics, general anesthetics, phenothiazines, tranquilizers, sedative-hypnotics, tricyclic antidepressants or other CNS depressants (including alcohol) concomitantly with DILAUDID may exhibit an additive CNS depression. When such combined therapy is contemplated, the dose of one or both agents should be reduced.

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