Opioid Antagonisten

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Opioid Antagonisten Einstellungen

Opioidantagonisten sind Rezeptorantagonisten der Opioidrezeptoren. Opioidantagonisten verdrängen nach Applikation das Opioid bzw. das Opiat mit der Folge, dass der Patient häufig schlagartig erwacht und sofort starke Entzugserscheinungen verspürt. Opioidantagonisten sind Rezeptorantagonisten der Opioidrezeptoren. Opioidantagonisten verdrängen nach Applikation das Opioid bzw. das Opiat (​Heroin. Opioidantagonisten sind Substanzen bzw. Arzneistoffe, die an Opioidrezeptoren wirken und dort die Wirkung der Opioide partiell oder komplett aufheben. Opioid-Antagonisten Arzneimittelgruppen. synonym: Morphin-Antagonisten, Opiat-Anagonisten. Wirkstoffe. Methylnaltrexon; Naldemedin; Nalmefen · Naloxon. Opioid-Antagonisten gegen süchtiges Verlangen. Mit Wirkstoffen zur Blockierung der Opioid-Rezeptoren im Gehirn versucht man das.

Opioid Antagonisten

Opioidantagonisten sind Substanzen bzw. Arzneistoffe, die an Opioidrezeptoren wirken und dort die Wirkung der Opioide partiell oder komplett aufheben. Opioid-Antagonisten Arzneimittelgruppen. synonym: Morphin-Antagonisten, Opiat-Anagonisten. Wirkstoffe. Methylnaltrexon; Naldemedin; Nalmefen · Naloxon. (Synthetische) Substanzen, die als kompetitive Antagonisten an Opioid-​Rezeptoren binden und damit die Wirkungen von Morphin und morphinartigen.

Opioid Antagonisten Aus dem Buch zitieren

Essenzielle Learn more here ermöglichen grundlegende Funktionen und sind für die einwandfreie Funktion der Website something Nsport Online excellent. Kategorie : Opioid. Die Daten dieser Studie wurden übrigens für mindestens eine weitere Publikation verwendet, in der es um die Zufriedenheit der Patienten ging 9. Oxycodon plus Naloxon deutlich diejenigen von Morphin Opioidantagonist Opioidantagonisten sind Medikamente, die eine starke Bindungsfähigkeit an die Opioidrezeptor im Zentralnervensystem besitzen. Seine noch nicht abgeschlossenen Untersuchungen zur Internetsucht wird Mann auch nach seiner offiziellen Verabschiedung am ZI weiterführen.

Opioid Antagonisten Video

Opioid Drugs, Part 1: Mechanism of Action

However, Alvimopan is indicated for perioperative management of postoperative ileus to accelerate the time to upper and lower GI recovery following surgery.

However, in the story of opioids, opioid antagonists may save lives. Naltrexone is an opioid antagonist that blocks the effects of opioids by competitive binding.

Naltrexone is indicated for alcohol and opioid dependence and useful because its opioid receptor blockade secondarily diminishes dopamine activity that is otherwise enhanced by alcohol.

The available formulations are Narcan nasal , Evzio Auto-injector , and solution for injection, the latter of which is frequently administered off label intranasally, by attaching an atomizer to the end of a syringe.

Although the chemistry behind opioids has been outlined, there are other parameters that also need to be factored in to determine individual response.

These include age, comorbidities, disease severity, gender, genetics, and weight, all of which may positively or negatively affect the drug response.

In addition to the pharmacodynamics outlined herein, many synthetic opioids have additional mechanisms of action, such as noradrenergic reuptake blockade and inhibition of n-methyl-D-aspartase NMDA receptors.

It is therefore important to consider all these variables when making decisions that affect opioid selection or discontinuation.

Opioid complications and side effects. Pain Physician. Pharmacology of opioids in the treatment of chronic pain syndromes.

Pain physician. Opioid receptors. Annu Rev Biochem. Nelson LS, Olsen D. Goldfrank's Toxicologic Emergencies. Talwin [prescribing information].

Bridgewater, NJ: Sanofi-aventis; Accessed January 5, Reversal of fentanyl related respiratory depression with nalbuphine.

Effects on the CO2-response curve in man. Acta Anaesthesiol Belg. Side effects of nalbuphine while reversing opioid-induced respiratory depression: report of four cases.

Can J Anaesth. Buprenex [prescribing information]. North Chesterfield, VA: Indivior; Butrans [prescribing information].

Stamford, CT: Purdue Pharma; Belbuca [prescribing information]. Malvern, PA: Endo Pharmaceuticals; Subutex [prescribing information].

Columbus, OH: Roxane Laboratories; Bunavail [prescribing information]. Suboxone [prescribing information].

Zubsolv [prescribing information]. Probuphine [prescribing information]. Lutfy K, Cowan A.

Buprenorphine: a unique drug with complex pharmacology. Curr Neuropharmacol. J Pharmacol Exp Ther.

Dahan A. Opioid-induced respiratory effects: new data on buprenorphine. Palliat Med. Journal of Psychopharmacology.

Journal of Clinical Psychopharmacology. Antidotes V03AB. Metadoxine , Thiamine. Bemegride Ethamivan. Cyprodenate Flumazenil. Physostigmine SCH Digoxin immune fab.

Dimercaprol Succimer. Calcium gluconate. Primary alcohols: Ethanol Fomepizole. Acetylcysteine Glutathione Methionine. Dimercaprol Edetates Prussian blue.

Copper sulfate Ipecacuanha Syrup of ipecac. Treatment of drug dependence N07B. Salvia divinorum. Opioid receptor modulators. Morphine may also cause nausea and vomiting by increasing gastrointestinal secretions and delaying passage of intestinal contents toward the colon.

Morphine depresses the vomiting center in the medulla. As a result, IV administration of morphine produces less nausea and vomiting than the intramuscular IM administration of morphine, presumably because opioid administered IV reaches the vomiting center as rapidly as it reaches the chemoreceptor trigger zone.

Nausea and vomiting are relatively uncommon in recumbent patients given morphine, suggesting that a vestibular component may contribute to opioid-induced nausea and vomiting.

Morphine can increase the tone and peristaltic activity of the ureter. In contrast to similar effects on biliary tract smooth muscle, the same opioid-induced effects on the ureter can be reversed by an anticholinergic drug such as atropine.

Urinary urgency is produced by opioid-induced augmentation of detrusor muscle tone, but, at the same time, the tone of the urinary sphincter is enhanced, making voiding difficult.

Antidiuresis that accompanies administration of morphine to animals has been attributed to opioid-induced release of arginine vasopressin hormone antidiuretic hormone.

In humans, however, administration of morphine in the absence of painful surgical stimulation does not evoke the release of this hormone.

Morphine causes cutaneous blood vessels to dilate. The skin of the face, neck, and upper chest frequently becomes flushed and warm.

These changes in cutaneous circulation are in part caused by the release of histamine. Histamine release probably accounts for urticaria and erythema commonly seen at the morphine injection site.

In addition, morphine-induced histamine release probably accounts for conjunctival erythema and pruritus. Localized cutaneous evidence of histamine release, especially along the vein into which morphine is injected, does not represent an allergic reaction.

Opioids are readily transported across the placenta. Therefore, depression of the neonate can occur as a consequence of administration of opioids to the mother during labor.

In this regard, maternal administration of morphine may produce greater neonatal depression than meperidine does.

Chronic maternal use of an opioid can result in the development of physical dependence in the fetus. Subsequent administration of naloxone to the neonate can precipitate neonatal abstinence syndrome.

The ventilatory depressant effects of some opioids may be exaggerated by amphetamines, phenothiazines, monoamine oxidase inhibitors, and tricyclic antidepressants.

For example, patients receiving monoamine oxidase inhibitors may experience exaggerated CNS depression and hyperpyrexia after administration of an opioid agonist, especially meperidine.

This exaggerated response may reflect alterations in the rate or pathway of metabolism of the opioid. Sympathomimetic drugs appear to enhance analgesia produced by opioids.

The cholinergic nervous system seems to be a positive modulator of opioid-induced analgesia in that physostigmine enhances and atropine antagonizes analgesia.

Prolonged opioid therapy may influence the hypothalamic-pituitary-adrenal axis and the hypothalamic-pituitary-gonadal axis, leading to endocrine and immune effects.

The main effects of opioids on the hypothalamic-pituitary-gonadal axis involve modulation of hormone release including increased prolactin and decreased luteinizing hormone, follicle-stimulating hormone, testosterone, and estrogen concentrations.

The principal manifestation of opioid overdose is depression of ventilation manifesting as a slow breathing frequency, which may progress to apnea.

Pupils are symmetric and miotic unless severe arterial hypoxemia is present, which results in mydriasis.

Skeletal muscles are flaccid, and upper airway obstruction may occur. Pulmonary edema commonly occurs, but the mechanism is not known.

Hypotension and seizures develop if arterial hypoxemia persists. The triad of miosis, hypoventilation, and coma should suggest overdose with an opioid.

Administration of an opioid antagonist to treat opioid overdose may precipitate acute withdrawal in dependent patients.

Paradoxically, preinduction administration of fentanyl, sufentanil, or alfentanil may be associated with significant reflex coughing.

Pharmacodynamic tolerance and physical dependence with repeated opioid administration are characteristics of all opioid agonists and are among the major limitations of their clinical use.

Cross-tolerance develops between all the opioids. Tolerance can occur without physical dependence, but the reverse does not seem to occur.

Tolerance is the development of the requirement for increased doses of a drug in this case, an opioid agonist to achieve the same effect previously achieved with a lower dose.

Such acquired tolerance usually takes 2 to 3 weeks to develop with analgesic doses of morphine, although acute tolerance can develop much more quickly with highly potent opioids.

The potential for physical dependence depends on the agonist effect of opioids. Indeed, physical dependence does not occur with opioid antagonists and is less likely with opioid agonist—antagonists.

When opioid agonist actions predominate, there often develops, with repeated use, both psychological and physiologic need for the drug.

Physical dependence on morphine usually requires about 25 days to develop but may occur sooner in emotionally unstable persons. Some degree of physical dependence, however, occurs after only 48 hours of continuous medication.

When physical dependence is established, discontinuation of the opioid agonist produces a typical withdrawal abstinence syndrome Table Insomnia and restlessness are prominent.

Abdominal cramps, nausea, vomiting, and diarrhea reach their peak in 72 hours and then decline over the next 7 to 10 days.

During withdrawal, tolerance to morphine is rapidly lost, and the syndrome can be terminated by a modest dose of opioid agonist.

The longer the period of abstinence, the smaller the dose of opioid agonist that will be required.

Pharmacodynamic tolerance has been related to neurologic changes that take place after long-term exposure to the opioid.

Opioid receptors on the cell membrane surfaces become gradually desensitized by reduced transcription and subsequent decreases in the absolute numbers of opioid receptors downregulation.

A second mechanism proposed to explain pharmacodynamic tolerance involves upregulation of the cAMP system.

Acutely, opioids inhibit functional activity of cAMP pathways by blocking adenylate cyclase, the enzyme that catalyzes the synthesis of cAMP.

Long-term opioid exposure is associated with gradual recovery of cAMP pathways and tolerance develops. Increased synthesis of cAMP may be responsible for physical dependence and physiologic changes associated with withdrawal.

Upregulation of cAMP has been most clearly demonstrated in the locus ceruleus of the brain. Tolerance is not due to enzyme induction, because no increase in the rate of metabolism of opioid agonists occurs.

Long-term pharmacodynamic tolerance characterized by opioid insensitivity may persist for months or years in some individuals and most likely represents persistent neural adaptation.

Prolonged exposure to opioids activates NMDA receptors via second messenger mechanisms and also downregulates spinal glutamate transporters.

The resultant high synaptic concentrations of glutamate and NMDA receptor activation contribute to opioid tolerance and abnormal pain sensitivity pronociceptive or sensitization process.

The observation that treatment with small doses of ketamine an NMDA receptor antagonist abolishes the acute opioid tolerance seen with remifentanil supports this hypothesis.

Opioid agonists include but are not limited to morphine, meperidine, fentanyl, sufentanil, alfentanil, and remifentanil see Table Opioid rotation may be useful when dose escalation is not effective in treating pain.

Isolated in and named after Morpheus, the Greek god of dreams, morphine is the prototype opioid agonist to which all other opioids are compared.

In humans, morphine produces analgesia, euphoria, sedation, and a diminished ability to concentrate. Other sensations include nausea, a feeling of body warmth, heaviness of the extremities, dryness of the mouth, and pruritus, especially in the cutaneous areas around the nose.

The cause of pain persists, but even low doses of morphine increase the threshold to pain and modify the perception of noxious stimulation such that it is no longer experienced as pain.

Continuous, dull pain is relieved by morphine more effectively than is sharp, intermittent pain. In contrast to nonopioid analgesics, morphine is effective against pain arising from the viscera as well as from skeletal muscles, joints, and integumental structures.

Analgesia is most prominent when morphine is administered before the painful stimulus occurs. Morphine is well absorbed after IM administration, with onset of effect in 15 to 30 minutes and a peak effect in 45 to 90 minutes.

The clinical duration of action is about 4 hours. Morphine is usually administered IV in the perioperative period, thus eliminating the unpredictable influence of drug absorption.

The peak effect equilibration time between the blood and brain after IV administration of morphine is delayed compared with opioids such as fentanyl and alfentanil, requiring about 15 to 30 minutes Table Morphine inhaled as an aerosol from a nebulizer may act on afferent nerve pathways in the airways to relieve dyspnea as associated with lung cancer and associated pleural effusion.

Cerebrospinal fluid CSF concentrations of morphine peak 15 to 30 minutes after IV injection and decay more slowly than plasma concentrations Fig.

Likewise, these same drug effects persist despite decreasing plasma concentrations of morphine. Moderate analgesia probably requires maintenance of plasma morphine concentrations of at least 0.

Only a small amount of administered morphine gains access to the CNS. For example, it is estimated that less than 0. Reasons for poor penetration of morphine into the CNS include a relatively poor lipid solubility, b high degree of ionization at physiologic pH, c protein binding, and d rapid conjugation with glucuronic acid.

Nevertheless, respiratory acidosis, which decreases the nonionized fraction of morphine, results in higher plasma and brain concentrations of morphine than are present during normocarbia Fig.

In contrast to the CNS, morphine accumulates rapidly in the kidneys, liver, and skeletal muscles. Morphine, unlike fentanyl, does not undergo significant first-pass uptake into the lungs.

Metabolism of morphine is primarily conjugation with glucuronic acid in hepatic and extrahepatic sites, especially the kidneys.

Morphineglucuronide is detectable in the plasma within 1 minute after IV injection, and its concentration exceeds that of unchanged drug by almost fold within 90 minutes Fig.

Morphineglucuronide is detectable in the urine for up to 72 hours after the administration of morphine. Renal metabolism makes a significant contribution to the total metabolism of morphine, which offers a possible explanation for the absence of any decrease in systemic clearance of morphine in patients with hepatic cirrhosis or during the anhepatic phase of orthotopic liver transplantation.

Elimination of morphine glucuronides may be impaired in patients with renal failure, causing an accumulation of metabolites and unexpected ventilatory depressant effects of small doses of opioids Fig.

After IV administration of morphine, the elimination of morphineglucuronide is somewhat longer than for morphine see Table and Fig. Plasma morphine concentrations are higher in the elderly than in young adults Fig.

Patients with renal failure exhibit higher plasma and CSF concentrations of morphine and morphine metabolites than do normal patients, reflecting a smaller volume of distribution Vd.

Concentrations of morphine in the colostrum of parturients receiving patient-controlled analgesia with morphine are low and it is unlikely that significant amounts of drug will be transferred to the breast-fed neonate.

Gender may affect opioid analgesia but the direction and magnitude of these differences depend on many interacting variables including the opioid used.

Likewise, morphine decreases the slope of the ventilatory response to carbon dioxide in women, whereas in men, there was no significant effect.

Hypoxic sensitivity is decreased by morphine in women but not men. Side effects described for morphine are also characteristic of other opioid agonists, although the incidence and magnitude may vary.

There are several analogues of meperidine, including fentanyl, sufentanil, alfentanil, and remifentanil. Meperidine shares several structural features that are present in local anesthetics including a tertiary amine, an ester group, and a lipophilic phenyl group.

Indeed, meperidine administered intrathecally blocks sodium channels to a degree comparable with lidocaine. Structurally, meperidine is similar to atropine, and it possesses a mild atropine-like antispasmodic effect on smooth muscle.

Meperidine is about one-tenth as potent as morphine.

Helfen die üblichen laxierenden Maßnahmen nicht, können durch die peripher angreifenden Opioid-Antagonisten Naloxon (in fixer Kombination mit Oxycodon. (Synthetische) Substanzen, die als kompetitive Antagonisten an Opioid-​Rezeptoren binden und damit die Wirkungen von Morphin und morphinartigen. (= O.) [engl. opioid antagonists; gr. ἀνταγωνιστής (antagonistes) Gegner], [PHA], Substanzen, die die Wirkung von Opioiden ganz oder teilweise antagonisieren. Opioidantagonist. Opioidantagonisten sind Medikamente, die eine starke Bindungsfähigkeit an die Opioidrezeptor im Zentralnervensystem besitzen. Je mehr ein. Weil Opioide ihre Wirkung über Rezeptoren vermitteln, sind spezifische Antagonisten auch in der Lage, diese Wirkungen kompetitiv, durch Verdrängung des. The duration of action of meperidine is 2 to 4 hours, making it a shorter acting opioid agonist than morphine. Entereg [prescribing information]. Normeperidine has an elimination half-time of 15 hours 35 hours in patients in renal failure and can be detected in urine for as long as 3 days after administration of meperidine. In this regard, physostigmine, which increases CNS levels of acetylcholine, may antagonize depression of ventilation but not analgesia produced by Beste in SС†lzerhС†fe finden. Although the chemistry behind opioids has been outlined, there are other parameters that also need to be factored in to determine individual response. In addition, morphine-induced histamine release probably accounts for conjunctival erythema and click here. Search x. Naltrexone is an opioid antagonist that blocks the effects of opioids by competitive binding.

Opioid Antagonisten - Inhaltsverzeichnis

Das erklärt man sich mit dem Endorphin-Entzug — vergleichbar einem Drogenentzug bei Suchtabhängigen. Wegen eines aktiven Metaboliten besteht aber möglicherweise die Gefahr von Interaktionen und Akkumulation bei Langzeitanwendung. Bei Nalmefen handelt es sich nicht um einen neuen Wirkstoff, sondern um eine neue Anwendung. Opioid Antagonisten McNicol, E. Diese Seite wurde zuletzt am Meinen Login an diesem Computer speichern. Pain13 Fachgebiete: Https://ladycup.co/online-casino-spiele-kostenlos/gaming-laptop-2020-test.php. Opioid Antagonisten

This guide will explain how opioid antagonists work and their use in medicine. Opioids and related drugs can fall into one of four categories based on their interaction with opioid receptors:.

Since the opioid system manages important functions like pain and mood, these compounds affect how your body works.

An opioid antagonist takes effect on someone who has opioids in their system. These medicines help many people with opioid addiction manage their symptoms or recover from an overdose.

Medical professionals and non-medical professionals can use naloxone to save the life of someone experiencing an opioid overdose.

Addiction recovery is a lifelong journey with many milestones along the way. Determining benchmarks or goals as you come out….

Since the late s, alcohol and drug-related deaths, as well as suicide, have steadily been on the rise for people….

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Industry Guide. Conference Coverage. Student Voices. When it comes to predicting therapeutic or adverse effects and efficacy , opioid-specific pharmacodynamics play a major role.

Pharmacodynamics, as we all well know, is the study of what a drug does to the body, including involvement with receptor binding and conformational changes that ultimately drive therapeutic and non-therapeutic effects ie, adverse effects.

Some of the adverse effects of opioids are listed in Table 1. Some of the receptors may be further divided into subtypes.

These receptors are important for expressing pain transmission and modulating pathways, including neurotransmission in the limbic system, midbrain, spinal cord, and thalamus.

Opioid receptors are ubiquitously present throughout the body, including but not limited to the gastrointestinal tract GI , immune cells, pituitary gland, and skin.

At these sites, opioid receptors carry out variable analgesic and non-analgesic functions. A summary of pharmacological and physiological effects for each opioid receptor is listed in Table 2.

Opioid receptors are 7 transmembrane spanning proteins that are coupled to inhibitory G-proteins.

When activated, they decrease adenyl cyclase production of the secondary messenger cyclic adenosine monophosphate. This causes a decrease in calcium influx from inhibition of voltage-gated calcium channels and results in the activation of potassium channels, which leads to hyperpolarization.

The hyperpolarized state causes inhibition of neuronal signaling, which in this case inhibits pain transmission.

These classifications are agonist, partial agonist, and antagonist. There are opioids that have dual agonist and antagonist functions.

Table 3. Examples of full agonists include codeine, fentanyl, heroin, hydrocodone, methadone, morphine, and oxycodone.

At low doses, both full and partial agonists may provide similar effects to their full agonist cousins.

However, when the dose of partial agonists increases, the analgesic activity will plateau, and further increases in doses will not provide additional relief but may increase the adverse effects.

Examples of partial agonists include buprenorphine, butorphanol, and tramadol. Examples include buprenorphine, butorphanol, nalbuphine, and pentazocine.

And, some opioids are agonists at 1 or more opioid receptors but also antagonists at other opioid receptors. Depression of cholinergic transmission in the CNS as a result of opioid-induced inhibition of acetylcholine release from nerve endings may play a prominent role in the analgesic and other side effects of opioid agonists.

Opioids do not alter responsiveness of afferent nerve endings to noxious stimulation nor do they block conduction of nerve impulses along peripheral nerves as opposed to local anesthetics.

The names of the three subtypes developed from the ligands originally found to bind to them or their tissue of origin mu— m orphine, kappa— k etocyclazocine, delta—isolated from mouse vas d eferens.

The opioid receptors have been cloned and their amino acid sequences defined. In the brain, opioid receptors are primarily found in the periaqueductal gray, locus ceruleus, and the rostral ventral medulla.

In the spinal cord, opioid receptors are found both on interneurons and primary afferent neurons in the dorsal horn. Consequently, direct application of opioid agonists to the spinal cord can produce intense analgesia.

Immune cells recruited to sites of inflammation also secrete opioid peptides to provide local analgesia. Functional and physical interactions between these receptor subtypes have been noted.

The logical reason for the existence of opioid receptors and endogenous opioid agonists is to function as an endogenous pain suppression system.

Once pain is consciously perceived, it has served its purpose and it is reasonable to posit that the ability to dampen this perception would have a survival benefit.

Opioid receptors are located in areas of the brain periaqueductal gray matter of the brainstem, amygdala, corpus striatum, and hypothalamus and spinal cord substantia gelatinosa that are involved with pain perception, integration of pain impulses, and responses to pain Fig.

As a result, neurons are hyperpolarized, which suppresses spontaneous discharges and evoked responses.

Analgesia induced by electrical stimulation of specific sites in the brain or mechanical stimulation of peripheral areas acupuncture most likely reflects release of endorphins.

In addition, a recent study demonstrated that positive treatment expectancy substantially enhanced doubled the analgesic benefit of remifentanil, whereas negative treatment expectancy abolished remifentanil analgesia.

The positive expectancy effects were associated with activity in the endogenous pain modulation system, and the negative expectancy effects with activity in the hippocampus.

An ideal opioid agonist would have a high specificity for receptors, producing desirable responses analgesia and little or no specificity for receptors associated with side effects.

To date, however, all opioids possess similar side effects that vary only in degree. Therefore, a focus on the effects of morphine provides a suitable starting point.

Morphine, even in large doses, given to supine and normovolemic patients is unlikely to cause direct myocardial depression or hypotension.

The same patients changing from a supine to a standing position, however, may manifest orthostatic hypotension and syncope, presumably reflecting morphine-induced impairment of compensatory sympathetic nervous system responses.

For example, morphine decreases sympathetic nervous system tone to peripheral veins, resulting in venous pooling and subsequent decreases in venous return, cardiac output, and blood pressure.

Morphine can also evoke decreases in systemic blood pressure due to drug-induced bradycardia or histamine release.

Morphine-induced bradycardia results from increased activity of the vagal nerves, which probably reflects stimulation of the vagal nuclei in the medulla.

Morphine may also exert a direct depressant effect on the sinoatrial node and acts to slow conduction of cardiac impulses through the atrioventricular node.

These actions, may, in part, explain decreased vulnerability to ventricular fibrillation in the presence of morphine.

Administration of opioids morphine, fentanyl in the preoperative medication or before the induction of anesthesia tends to slow heart rate during exposure to volatile anesthetics with or without surgical stimulation.

Opioid-induced histamine release and associated hypotension are variable in both incidence and severity. The magnitude of morphine-induced histamine release and subsequent decrease in systemic blood pressure can be minimized by a limiting the rate of morphine infusion to 5 mg per minute intravenously IV , b maintaining the patient in a supine to slightly head-down position, and c optimizing intravascular fluid volume.

Pretreatment of patients with H 1 and H 2 receptor antagonists does not alter release of histamine evoked by morphine but does prevent changes in systemic blood pressure and systemic vascular resistance.

Morphine does not sensitize the heart to catecholamines or otherwise predispose to cardiac dysrhythmias as long as hypercarbia or arterial hypoxemia does not result from ventilatory depression.

Tachycardia and hypertension that occur during anesthesia with morphine are not pharmacologic effects of the opioid but rather are responses to painful surgical stimulation that are not suppressed by morphine.

Both the sympathetic nervous system and the renin-angiotensin axis contribute to these cardiovascular responses.

Large doses of morphine or other opioid agonists may decrease the likelihood that tachycardia and hypertension will occur in response to painful stimulation, but once this response has occurred, administration of additional opioid is unlikely to be effective.

During anesthesia, however, opioids are commonly administered with inhaled or IV anesthetics to ensure amnesia. The combination of an opioid agonist such as morphine or fentanyl with nitrous oxide results in cardiovascular depression decreased cardiac output and systemic blood pressure plus increased cardiac filling pressures , which does not occur when either drug is administered alone.

Opioids have been increasingly recognized as playing a role in protecting the myocardium from ischemia.

All opioid agonists produce dose-dependent and gender-specific depression of ventilation, primarily through an agonist effect at mu 2 receptors leading to a direct depressant effect on brainstem ventilation centers.

Opioid-induced depression of ventilation is characterized by decreased responsiveness of these ventilation centers to carbon dioxide as reflected by an increase in the resting Pa CO 2 and displacement of the carbon dioxide response curve to the right.

Opioid agonists also interfere with pontine and medullary ventilatory centers that regulate the rhythm of breathing, leading to prolonged pauses between breaths and periodic breathing.

It is possible that opioid agonists diminish sensitivity to carbon dioxide by decreasing the release of acetylcholine from neurons in the area of the medullary ventilatory center in response to hypercarbia.

In this regard, physostigmine, which increases CNS levels of acetylcholine, may antagonize depression of ventilation but not analgesia produced by morphine.

Depression of ventilation produced by opioid agonists is rapid and persists for several hours, as demonstrated by decreased ventilatory responses to carbon dioxide.

High doses of opioids may result in apnea, but the patient remains conscious and able to initiate a breath if asked to do so.

Death from an opioid overdose is almost invariably due to depression of ventilation. Clinically, depression of ventilation produced by opioids manifests as a decreased frequency of breathing that is often accompanied by a compensatory increase in tidal volume.

The incompleteness of this compensatory increase in tidal volume is evidenced by predictable increases in the Pa CO 2.

Many factors influence the magnitude and duration of depression of ventilation produced by opioid agonists.

For example, advanced age and the occurrence of natural sleep increase the ventilatory depressant effects of opioids.

Conversely, pain from surgical stimulation counteracts depression of ventilation produced by opioids. Likewise, the analgesic effect of opioids slows breathing that has been rapid and shallow due to pain.

Opioids produce dose-dependent depression of ciliary activity in the airways. Increases in airway resistance after administration of an opioid are probably due to a direct effect on bronchial smooth muscle and an indirect action due to release of histamine.

Opioids depress cough by effects on the medullary cough centers that are distinct from the effects of opioids on ventilation.

The greatest cough suppression occurs with opioids that have bulky substitutions at the number 3 carbon position codeine.

One useful property of dextrorotatory isomers such as dextromethorphan is that they can suppress cough but do not produce analgesia or depression of ventilation.

Thus, in some cases, opioids can be safely sold over-the-counter. In the absence of hypoventilation, opioids decrease cerebral blood flow and possibly intracranial pressure ICP.

These drugs must be used with caution in patients with head injury because of their a associated effects on wakefulness, b production of miosis, and c depression of ventilation with associated increases in ICP if the Pa CO 2 becomes increased.

Furthermore, head injury may impair the integrity of the blood—brain barrier, with resultant increased sensitivity to opioids.

The effect of morphine on the electroencephalogram EEG resembles changes associated with sleep. Opioids do not alter the responses to neuromuscular blocking drugs.

Skeletal muscle rigidity, especially of the thoracic and abdominal muscles, is common when large doses of opioid agonists are administered rapidly and intravenously.

Miosis is due to an excitatory action of opioids on the autonomic nervous system component of the Edinger-Westphal nucleus of the oculomotor nerve.

Tolerance to the miotic effect of morphine is not prominent. Miosis can be antagonized by atropine, and profound arterial hypoxemia in the presence of morphine can still result in mydriasis.

Rapid IV administration of large doses of an opioid particularly fentanyl and its derivatives as used in cardiac surgery can lead to generalized skeletal muscle rigidity.

This can be severe enough to interfere with manual ventilation. Although generally termed chest wall rigidity, evidence supports the conclusion that the majority of resistance to ventilation is due to laryngeal musculature contraction.

Postoperative titration of morphine frequently induces sedation that precedes the onset of analgesia. The assumption that sleep occurs when pain is relieved is not necessarily accurate and morphine-induced sedation should not be considered as an indicator of appropriate analgesia during IV morphine titration.

Opioids can cause spasm of biliary smooth muscle, resulting in increases in biliary pressure that may be associated with epigastric distress or biliary colic.

This pain may be confused with angina pectoris. Naloxone will relieve pain caused by biliary spasm but not myocardial ischemia.

Conversely, nitroglycerin will relieve pain due to either biliary spasm or myocardial ischemia. It may be necessary to reverse opioid-induced biliary smooth muscle spasm with naloxone so as to correctly interpret the cholangiogram.

Glucagon, 2 mg IV, also reverses opioid-induced biliary smooth muscle spasm and, unlike naloxone, does not antagonize the analgesic effects of the opioid.

Contraction of the smooth muscles of the pancreatic ducts is probably responsible for increases in plasma amylase and lipase concentrations that may be present after the administration of morphine.

Such increases may confuse the diagnosis when acute pancreatitis is a possibility. Commonly used opioids such as morphine, meperidine, and fentanyl can produce spasm of the gastrointestinal smooth muscles, resulting in a variety of side effects including constipation, biliary colic, and delayed gastric emptying.

Morphine decreases the propulsive peristaltic contractions of the small and large intestines and enhances the tone of the pyloric sphincter, ileocecal valve, and anal sphincter.

The delayed passage of intestinal contents through the colon allows increased absorption of water. As a result, constipation often accompanies therapy with opioids and may become a debilitating problem in patients who require chronic opioid therapy, as little tolerance develops to this effect.

Of interest, opium was used to treat diarrhea before its use as an analgesic was popularized. Increased biliary pressure occurs when the gallbladder contracts against a closed or narrowed sphincter of Oddi.

Passage of gastric contents into the proximal duodenum is delayed because there is increased tone at the gastroduodenal junction.

In this regard, preoperative medication that includes an opioid could slow gastric emptying potentially increase the risk of aspiration or delay the absorption of orally administered drugs.

Opioid-induced nausea and vomiting are caused by direct stimulation of the chemoreceptor trigger zone in the floor of the fourth ventricle.

This may reflect the role of opioid agonists as partial dopamine agonists at dopamine receptors in the chemoreceptor trigger zone.

Indeed, apomorphine is a profound emetic and is also the most potent of the opioids at dopamine receptors. Stimulation of dopamine receptors as a mechanism for opioid-induced nausea and vomiting is consistent with the antiemetic efficacy of butyrophenones and phenothiazines.

Morphine may also cause nausea and vomiting by increasing gastrointestinal secretions and delaying passage of intestinal contents toward the colon.

Morphine depresses the vomiting center in the medulla. As a result, IV administration of morphine produces less nausea and vomiting than the intramuscular IM administration of morphine, presumably because opioid administered IV reaches the vomiting center as rapidly as it reaches the chemoreceptor trigger zone.

Nausea and vomiting are relatively uncommon in recumbent patients given morphine, suggesting that a vestibular component may contribute to opioid-induced nausea and vomiting.

Morphine can increase the tone and peristaltic activity of the ureter. In contrast to similar effects on biliary tract smooth muscle, the same opioid-induced effects on the ureter can be reversed by an anticholinergic drug such as atropine.

Urinary urgency is produced by opioid-induced augmentation of detrusor muscle tone, but, at the same time, the tone of the urinary sphincter is enhanced, making voiding difficult.

Antidiuresis that accompanies administration of morphine to animals has been attributed to opioid-induced release of arginine vasopressin hormone antidiuretic hormone.

In humans, however, administration of morphine in the absence of painful surgical stimulation does not evoke the release of this hormone.

Morphine causes cutaneous blood vessels to dilate. The skin of the face, neck, and upper chest frequently becomes flushed and warm.

These changes in cutaneous circulation are in part caused by the release of histamine.

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