The hydrochloride salt of the semi-synthetic opioid hydromorphone with analgesic activity.
Hydromorphone, the hydrogenated ketone of morphine, selectively binds the mu-opioid receptor, a G protein-coupled receptor. Binding stimulates the exchange of guanosine triphosphate (GTP) for guanosine diphosphate (GDP) on the G-protein complex, resulting in inhibition of plasma membrane-associated adenylate cyclase (AC) and a reduction in intracellular cyclic 3',5'-adenosine monophosphate (cAMP) levels. Due to a reduction in cAMP levels, voltage-gated potassium channels are activated, resulting in neuronal hyperpolarization and a reduction in neuronal excitability. In addition, this agent inhibits the opening of voltage-gated calcium channels, resulting in inhibition of calcium entry into neuronal cells and a reduction in the release of nociceptive neurotransmitters such as substance P and glutamate.
Analgesia opioid naive patients: 2-4 mg 4-6 hrly. Usual: 2-8 mg 3-4 hrly. Higher doses may be needed in opioid experienced patients.
Cough suppressant: 1 mg 3-4 hrly.
Analgesia: 1-2 mg 4-6 hrly.
Analgesia - supp: 3 mg 6-8 hrly.
Adverse drug reactions: GI disturbances, difficulty with micturition, CV effects, hypothermia, hallucinations, dysphoria, mood changes, dependence, miosis, decreased libido or potency, hypersensitivity reactions. Respiratory depression and hypotension may occur with larger doses.