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Morphine is the archetypal opioid analgesic. Because it is a short-acting opioid, its use has been limited to the management of acute pain. The development of extended-release formulations have resulted in the increased utilization of morphine in chronic pain conditions.

This review documents the history of morphine use in pain treatment, and describes the metabolism, pharmacodynamics, formulations, and efficacy of the currently available extended-release morphine medications. Morphine was the first, and in many ways, the Kadian 30 important opioid used to treat Kadian 30 and cancer pain. However, morphine is a short-acting medication, and Kadian 30 frequency of administration necessary to maintain adequate blood levels made it difficult to use this agent in the chronic setting.

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It Kadian 30 not until morphine was available in a long-acting formulation that it became used for chronic, noncancer pain. With Kadian 30 or twice a day dosing, steady-state blood levels can be achieved, compliance can Kadian 30 improved, and patients can sleep through the night.

There should also, theoretically, be less reinforcement of drug misuse behavior, although that has never been proven. Opioids have been used for their euphoric and analgesic properties for thousands of years.

Morphine has a risk for...

Ancient records indicate that it was also Kadian 30 by the Assyrians, Babylonians, and Egyptians. He accomplished this by boiling the poppy plant and precipitating crystals from the water using ammonia, yielding a water-insoluble crystal.

Although Serturner is known as the scientist who first isolated morphine, it was not until that Robert Robinson deduced the empiric formula, and in it was synthesized in the laboratory by Marshal T Cates, Jr. Alkaloids are natural occurring, nitrogen-containing bases found in plants. The opioid receptors were first discovered in6 and the first endogenous opioid enkephalin was subsequently discovered in Mu receptors are found primarily in the brainstem and medial thalamus.

Activation of these receptors can result in supraspinal analgesia, respiratory depression, euphoria, sedation, decreased gastrointestinal GI motility, and physical dependence.

The subtype Mu-1 is mostly associated with analgesia, euphoria, Kadian 30 serenity, while Mu-2 is related to respiratory depression, pruritus, prolactin release, dependence, anorexia, and sedation. Kappa receptors are found in the limbic and other diencephalic areas, brainstem, and spinal cord, and are responsible for spinal analgesia, sedation, dyspnea, dependence, dysphoria, and respiratory depression.

Delta receptors are located largely in the brain and their effects are not well studied. Currently, activation of delta receptors is thought to Kadian 30 responsible for psychomimetic and dysphoric effects.

This medication is used to...

These opioid receptors are G-linked proteins embedded in the cell membrane. When the opioid attaches to the receptor, the receptor is activated, releasing a portion of the G protein, which diffuses within the cytoplasm until it reaches its target either an Kadian 30 or an ion channel.

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Opioid receptors located on the presynaptic terminals of nociceptive C fibers and A delta fibers, when activated by an opioid agonist, will indirectly inhibit voltage-dependent calcium channels, thereby decreasing cAMP levels and blocking the release of pain neurotransmitters such as glutamate, substance P, and calcitonin gene-related peptide from the nociceptive fibers, resulting in analgesia Figure 2.

Opioids and endogenous opioids also activate presynaptic Kadian 30 on gamma aminobutyric Kadian 30 GABA neurons, which inhibit the release of GABA in the Kadian 30 tegmental area 10 Figure 3. The inhibition of GABA allows dopaminergic neurons to fire more vigorously, and the extra dopamine in the nucleus accumbens is intensely pleasurable. The basic morphine compound in its raw form exists as a bitter, white crystalline compound that is water-insoluble.

It is designated with the chemical formula C 17 H 19 NO 3. Pharmaceutical-grade morphine exists as a salt, typically in the form Kadian 30 morphine hydrochloride, morphine acetate, or morphine sulfate Figure 4. Morphine has very poor lipid solubility, undergoes rapid conjugation with glucuronic acid, ionizes at physiologic pH and becomes highly protein-bound after oral administration.

It takes approximately 30 minutes for the immediate-release morphine formulation to reach the central nervous system, and Kadian 30 minutes for the extended-release formulation. Once absorbed, morphine is distributed to skeletal muscle, kidneys, liver, intestinal tract, lungs, spleen, and brain. Morphine also crosses the placental membrane and has been found in breast milk. The nonalkalinized form of morphine Kadian 30 the blood-brain barrier more readily than the alkalinized form.

Kadian 30 of the blood increases the fraction of nonionized morphine, thereby enhancing delivery Kadian 30 the central nervous system. During respiratory acidosis, brain concentrations of morphine increase because of increased cerebral blood flow secondary to higher carbon dioxide tension, which facilitates delivery of the nonionized form through the blood-brain barrier. Glucuronidation Kadian 30 morphine occurs immediately after it is absorbed into the serum at both hepatic and extrahepatic sites.

One of the most feared side effects of morphine is that of respiratory depression, with subsequent potential respiratory arrest.

Morphine sulfate is an agonist...

Morphine also leads to decreased sympathetic tone, resulting in venous pooling and orthostatic hypotension. Effects on the GI and genitourinary systems include spasm of biliary smooth muscle, sphincter of Oddi spasm, Kadian 30 intestinal motility with constipation, direct stimulation of the Kadian 30 receptor trigger zone in the floor of the fourth ventricle resulting in nausea and vomiting, and spasm of the bladder trigone with urinary retention. Morphine Kadian 30 also associated with direct histamine release, which can lead to bronchospasm, hypertension, peripheral vasodilatation, flushing of the skin, and urticaria.

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All opioids are associated with the risk of addiction, tolerance, dependence, and hyperalgia. Because opioids increase dopamine levels in the brain, they produce a pleasurable sensation, which is felt to be addictive. These dopamine centers are also the site of action Kadian 30 the addictive actions of alcohol, nicotine, and cocaine.

This has led to a dramatic increase in opioid prescribing, including extended-release morphine, with a Kadian 30 increase in opioid poisonings and death.

The benefit of analgesia, therefore, must always be balanced with the risk of addiction and overdose. Tolerance, ie, loss of analgesic potency, leads to increasing dose requirements. The opioid receptors can become upregulated by continued exposure to the medication, or the enzymes controlling metabolism Kadian 30 be induced by prolonged exposure. Hyperalgia or hyperalgesia is defined as increased pain Kadian 30 in the setting of Kadian 30 increased opioid dose. Morphine had a limited impact on medical science until the invention of the hypodermic needle by a Scottish physician, Alexander Wood, sometime between and The subsequent development of a commercially available oral form of morphine heralded the discipline of Kadian 30 pain medicine as we Kadian 30 know it.

Major advances in the pharmacotherapy of chronic pain have led to the development of Kadian 30 opioid delivery systems, thereby allowing less frequent dosing than the classic short-acting formulas.

It is the Kadian 30 in serum drug levels that define the difference between short-acting opioids SAO and long-acting opioids LAO ; with SAOs, serum opioid levels rise rapidly following administration and then decline rapidly, while LAO administration allows for less fluctuation in serum opioid levels and an extended period within the therapeutic range.

Kadian 30 are many proposed advantages of the long-acting formula compared with the short-acting formula. Several studies have suggested that modified-release opioids may result in fewer side effects than have been observed with short-acting opioids.

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The modified-release opioids have been preferred over the short-acting opioids because of the longer duration of action, which lessens Kadian 30 frequency and severity of end-of-dose pain.

However, in a recent systematic review of long-acting versus short-acting opioids, 24 Rauck noted that, while it was clear that long-acting opioids achieved more stable drug levels, there was no clear evidence from appropriately designed comparative trials to make a case for the use of one type of formulation over the Kadian 30 on Kadian 30 basis of clinical efficacy.

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Several extended-release oral morphine formulations are now commercially available. The dose intervals recommended for these formulations vary from 8 to 12 to 24 hours. The morphine sulfate in MSContin is contained in a dual-action polymer mix consisting of a Kadian 30 polymer hydroxypropyl methylcellulose and a hydrophobic polymer hydroxyethyl cellulosecetostearyl alcohol, hypromellose, magnesium stearate, polyethylene glycol, talc, and titanium dioxide.

The rate of drug release from this formulation depends on the rate of Kadian 30 of the dissolved morphine through the gel layer at the surface of the tablet.

The depth of the gel layer increases over time as the gastric fluid gains access to the deeper regions of the Kadian 30. The release rate can be controlled by varying the hydrophilic polymer, the type of hydrophobic matrix, or their ratio. A suspension formula of MSContin is also available.


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