Central nervous system opioids causing

Analgesics are classed as narcotic (which act in the central nervous system and cause drowsiness, i.e. opioids) and non-narcotic (which act chiefly peripherally, e.g. diclofenac). 

The most commonly abused prescription drugs are opioids and opiates such as oxycodone and morphine, central nervous system depressants such as barbiturates and benzodiazepines, and stimulants such as dextroamphetamine and methylphenidate. Brand-name painkillers such as Vicodin and OxyContin, depressants such as Valium and Xanax, and stimulants such as Ritalin and Dexedrine are commonly abused (as are some OTC cough remedies). Although helpful and safe when used appropriately, these drugs can cause serious harm when taken in unapproved ways. 

Opioids are compounds that bind one or more of the many different opioid receptors in the body. Opioids act primarily on the central nervous system. The selectivity of a given opioid for the various opioid receptors determines its characteristic activity. While many opioids are powerful analgesics, opioids often cause physical dependence and have tolerance issues. Sedation and decreased rate of breathing are also side effects associated with opioids. Despite their problems, opioids are generally the drug of choice for treating severe, acute pain. 

Such events show how the immune, endocrine and central nervous systems are integrated in their responses to any form of stress. It is well established that physical or psychosocial stress causes increased secretions of prolactin, growth hormones, thyroid, and gonadal hormones, in addition to ACTH. Endogenous opioids are secreted under such conditions and function as immunomodulators, while also elevating the pain threshold. Receptors for such hormones exist on immunocompetent cells, along with receptors for catecholamines, serotonin and acetylcholine. 

Drugs and chemicals are known to cause activated interaction. The depressant action of opioid drugs is enhanced by drugs acting on the central nervous system (CNS) such as alcohol, anesthetics, anxiolytics, hypnotics, tricyclic antidepressants, and antipsychotics. Concomitant administration of opioid analgesics and monoamine oxidase inhibitors (MAOIs) should be avoided, or extra care should be taken if such a therapy is inevitable. Fatal reactions are reported when treated along with selegiline. Interactions also are reported with cyclizine, cimetidine, mexiletine, cisapride, metoclopramide, or domperidone. 

The main adverse effects of the opioid antagonists fall into two groups. The first are those caused by a reversal of opioid actions these include hypotension, pulmonary edema, atrial and ventricular dysrhythmias, and cardiac arrest. The risk of such effects is increased in patients with pre-existing cardiac abnormalities. The second group of effects results from direct actions of the opioid antagonists and their actions on the central nervous system, that is typical opioid effects, including dependence. 

The mechanism of loperamide toxicity is related to opioid-like activity that causes depression of the central nervous system (CNS). The abuse potential for loperamide is low. 

Its mechanism of action is similar to morphine and it stimulates a number of specific opioid receptors in the brain, causing central nervous system (CNS) and respiratory depression. 

Drug interactions morphine has additive effects when used in conjunction with alcohol, other opioids, or illicit drugs that cause central nervous system depression because respiratory depression, hypotension, and profound sedation or coma may result. 

Hydrocodone and oxycodone are widely prescribed opioid analgesics that are agonists at the mu, kappa, and delta receptors in the central nervous system. The cellular changes that occur with agonism at the opioid receptors are still under investigation. However, it is known that mu opioid receptors are G protein-coupled receptors that decrease intracellular levels of cAMP. This decrease in intracellular cAMP inhibits the release of critical neurotransmitters and hormones including substance P, acetylcholine, GABA, somatostatin, and other substances that activate or sensitize nociceptors. Inhibition of neurotransmitter release causes a subsequent decrease in the perceived level of pain by the patient. Also, activation of opioid receptors modifies specific calcium channels at the surface of cells, which hyperpolarizes and decreases excitability of neurons. 

Hydromorphone binds to mu and delta opiod receptors in the central nervous system. It has no effect at the kappa, sigma, or epsilon opioid receptors. Activity at the mu receptors causes analgesia, but also miosis, urinary retention, constipation, hyperthermia, and euphoria. Other side effects such as respiratory depression, pruritus, nausea, vomiting, and development of tolerance are due to binding at both mu and delta receptors. Hydromorphone, unlike other opioids, also has a direct depressant effect on the respiratory brainstem center and the cough center in the medulla. 

Morphine is perhaps the most extensively used analgesic for the management of acute pain associated with injury, neuropathic conditions and cancer. Morphine acts on the central nervous system by activating membrane opioid receptors. The pharmacological effects of morphine vary enormously with dosage. Small doses induce euphoria and sedation, whereas high doses cause pupil dilation, irregular respiration, pale skin, a deep sleep and eventual death within 6-8 h due to respiratory paralysis (Hesse 2002). Even at moderate doses, morphine causes constipation, loss of appetite, hypothermia, a slow... 

Opioid drugs act at opioid receptors distributed throughout the central/peripheral nervous system, causing a wide range of physiological, behavioural and cognitive effects. The main adverse drug interactions are due to additive depressive effects on the CNS, which results in loss of consciousness, respiratory depression and hypotension. 

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