What do opioids cause

These symptoms can be minimized through measures such as a slow reduction in dosage, consultation with the appropriate specialists, and psychological support for anxiety. While withdrawal symptoms can be difficult to endure, they can be managed effectively with positive results, especially with the assistance of a specialist like a physician anesthesiologist. According to the Centers for Disease Control and Prevention, most people have improved function without worsening pain after stopping opioid use.

Some patients have even experienced improved pain relief after weaning off the medicine, even though pain might briefly get worse at first. Additionally, alternative therapies with fewer risks and side effects may be effective in managing pain.

Because opioids mask pain, removing them can also give the pain management specialist a better understanding of the nature and level of your discomfort. With that understanding, the physician can better assess which alternative treatments could be effective for you. Physician anesthesiologists are the most highly skilled medical experts in anesthesia care, pain management, and critical care medicine, with the education and training that can mean the difference between life and death.

Skip to content. What are opioids? How do opioids work? What are the potential side effects? Side effects of opioids include: Sleepiness Constipation Nausea Opioids can also cause more serious side effects that can be life-threatening. The following might be symptoms of an opioid overdose and should be reported to a doctor immediately: Shallow breathing Slowed heart rate Loss of consciousness In addition, if you suddenly stop taking opioids, you can sometimes experience symptoms such as jittery nerves or insomnia.

Are there different types of opioids? There are many types of prescribed opioids that are known by several names, including: Codeine Fentanyl Hydrocodone Oxycodone Oxymorphone Morphine These medications are often sold under brand names such as OxyContin, Percocet, Palladone, and Vicodin. Heroin is an illegal and highly addictive form of opioid with no sanctioned medical use.

View generational differences on opioid use PDF How are opioids taken? How can you safely use opioids to manage pain? If opioids remain the best option, ask how to minimize the risks and side effects.

Provide information on your medical conditions — and if you have taken opioids in the past, tell your physician how they affected you. Also tell your physician if you have a history of addiction to drugs or alcohol; people predisposed to alcohol abuse may be more susceptible to misusing opioids.

Opioid addiction can cause life-threatening health problems, including the risk of overdose. Overdose occurs when high doses of opioids cause breathing to slow or stop, leading to unconsciousness and death if the overdose is not treated immediately. Both legal and illegal opioids carry a risk of overdose if a person takes too much of the drug, or if opioids are combined with other drugs particularly tranquilizers called benzodiazepines. Misuse of prescription opioids and heroin affects more than 2 million Americans and an estimated 15 million people worldwide each year.

The prevalence of opioid misuse and addiction is rapidly increasing. In , more than 20, deaths in the United States were caused by an overdose of prescription opioids, and another 13, deaths resulted from heroin overdose. Drug overdoses are now the leading cause of death in U. The causes of opioid addiction are complex. This condition results from a combination of genetic, environmental, and lifestyle factors, some of which have not been identified.

Many of the genes that are thought to play a role in opioid addiction are involved in the endogenous opioid system, which is the body's internal system for regulating pain, reward, and addictive behaviors. It consists of opioid substances produced naturally within the body called endogenous opioids and their receptors, into which opioids fit like keys into locks. Opioids introduced from outside the body called exogenous opioids , including opioid medications and heroin, also exert their effects by acting on these receptors.

Variations in the genes that provide instructions for making opioid receptors have been studied extensively as genetic risk factors for opioid addiction. Researchers suspect that differences in the receptors' structure and function influence how the body responds to opioids.

Opioid receptors are found in the nervous system, where they are embedded in the outer membrane of nerve cells neurons. When endogenous or exogenous opioids attach bind to the receptors, the interaction triggers a series of chemical changes within and between neurons that leads to feelings of pleasure and pain relief.

Common variations in the OPRM1 gene appear to influence how the body responds to opioids, including the amount of an opioid medication needed to achieve pain relief. At least in some populations, these variations have also been associated with the risk of opioid addiction. Variations in genes involved in other aspects of nervous system function have also been studied as risk factors for opioid addiction.

Some of these genes play roles in various neurotransmitter pathways, in which chemicals called neurotransmitters and their receptors relay signals from one neuron to another. Other genes provide instructions for proteins that help control the growth, survival, and specialization differentiation of neurons. These memories, called conditioned associations, often lead to the craving for drugs when the abuser reen-counters those persons, places, or things, and they drive abusers to seek out more drugs in spite of many obstacles.

When drugs stimulate mu opioid receptors in the brain, cells in the ventral tegmental area VTA produce dopamine and release it into the nucleus accumbens NAc , giving rise to feelings of pleasure. Feedback from the prefrontal cortex PFC to the VTA helps us overcome drives to obtain pleasure through actions that may be unsafe or unwise, but this feedback appears to be compromised in individuals who become addicted to drugs. The locus ceruleus LC is an area of the brain that plays an important role in drug dependence.

However, the compulsion to use opioids builds over time to extend beyond a simple drive for pleasure. This increased compulsion is related to tolerance and dependence. From a clinical standpoint, opioid withdrawal is one of the most powerful factors driving opioid dependence and addictive behaviors. Repeated exposure to escalating dosages of opioids alters the brain so that it functions more or less normally when the drugs are present and abnormally when they are not.

Two clinically important results of this alteration are opioid tolerance the need to take higher and higher dosages of drugs to achieve the same opioid effect and drug dependence susceptibility to withdrawal symptoms. Withdrawal symptoms occur only in patients who have developed tolerance. Opioid tolerance occurs because the brain cells that have opioid receptors on them gradually become less responsive to the opioid stimulation.

For example, more opioid is needed to stimulate the VTA brain cells of the mesolimbic reward system to release the same amount of DA in the NAc.

Therefore, more opioid is needed to produce pleasure comparable to that provided in previous drug-taking episodes. Opioid dependence and some of the most distressing opioid withdrawal symptoms stem from changes in another important brain system, involving an area at the base of the brain—the locus ceruleus LC Figure 2. Neurons in the LC produce a chemical, noradrenaline NA , and distribute it to other parts of the brain where it stimulates wakefulness, breathing, blood pressure, and general alertness, among other functions.

With repeated exposure to opioids, however, the LC neurons adjust by increasing their level of activity. Now, when opioids are present, their suppressive impact is offset by this heightened activity, with the result that roughly normal amounts of NA are released and the patient feels more or less normal.

The locus ceruleus LC is an area of the brain that is critically involved in the production of opioid dependence and withdrawal.

The diagrams show how opioid drugs affect processes in the LC that control the release of noradrenaline NA , a brain chemical that stimulates wakefulness, muscle tone, and respiration, among other functions.

Normally, natural opiatelike chemicals produced by the body link to mu opioid receptors on the surface of neurons. This linkage activates an enzyme that converts a chemical called adenosine triphosphate ATP into another chemical, called cyclic adenosine monophosphate cAMP , which in turn triggers the release of NA.

Prior to initiation of opioid drug abuse, the neuron produces enough NA to maintain normal levels of alertness, muscle tone, respiration, etc.

When heroin or another opioid drug links to the mu opioid receptors, it inhibits the enzyme that converts ATP to cAMP. Alertness, muscle tone, and respiration drop, and the acute opioid effects of sedation, shallow breathing, etc. With repeated heroin exposure, the neuron increases its supply of enzyme and ATP molecules. Using these extra raw materials, the neuron can produce enough cAMP to offset the inhibitory effect of the drug and release roughly normal amounts of NA despite the presence of the drug.

At this stage, the individual no longer experiences the same intensity of acute opioid effects as in earlier stages of abuse.

Operating at normal efficiency but with enhanced supplies of converting enzyme and ATP, the neuron produces abnormally high levels of cAMP, leading to excessive release of NA. The patient experiences the clinical symptoms of withdrawal—jitters, anxiety, muscle cramps, etc. If no further drugs are taken, the neuron will largely revert to its predrug condition panel A within days or weeks.

Other brain areas in addition to the LC also contribute to the production of withdrawal symptoms, including the mesolimbic reward system. These changes in the VTA and the DA reward systems, though not fully understood, form an important brain system underlying craving and compulsive drug use. Subsequently, repeated exposure to opioid drugs induces the brain mechanisms of dependence, which leads to daily drug use to avert the unpleasant symptoms of drug withdrawal.

Further prolonged use produces more long-lasting changes in the brain that may underlie the compulsive drug-seeking behavior and related adverse consequences that are the hallmarks of addiction. Recent scientific research has generated several models to explain how habitual drug use produces changes in the brain that may lead to drug addiction.

In reality, the process of addiction probably involves components from each of these models, as well as other features. GABA gamma-amino butyric acid : A neurotransmitter in the brain whose primary function is to inhibit the firing of neurons. The basic idea is that drug abuse alters a biological or physiological setting or baseline. Koob and LeMoal suggest that opioids cause addiction by initiating a vicious cycle of changing this set point such that the release of DA is reduced when normally pleasurable activities occur and opioids are not present.

Similarly, a change in set point occurs in the LC, but in the opposite direction, such that NA release is increased during withdrawal, as described above. Under this model, both the positive drug liking and negative drug withdrawal aspects of drug addiction are accounted for.

Activation of opioid receptors by heroin and heroin-like drugs initially bypasses these brakes and leads to a large release of DA in the NAc. However, with repeated heroin use, the brain responds to these successive large DA releases by increasing the number and strength of the brakes on the VTA DA neurons.

When this happens, the dependent addict will take even more heroin to offset the reduction of normal resting DA release. When he or she stops the heroin use, a state of DA deprivation will result, manifesting in dysphoria pain, agitation, malaise and other withdrawal symptoms, which can lead to a cycle of relapse to drug use.

A third variation on the set-point change emphasizes the sensitivity to environmental cues that leads to drug wanting or craving rather than just reinforcement and withdrawal Breiter et al.

During periods when the drug is not available to addicts, their brains can remember the drug, and desire or craving for the drug can be a major factor leading to drug use relapse. This craving may represent increased activity of the cortical excitatory glutamate neurotransmitters, which drive the resting activity of the DA-containing VTA neurons, as mentioned, and also drive the LC NA neurons. As the glutamate activity increases, DA will be released from the VTA, leading to drug wanting or craving, and NA will be released from the LC, leading to increased opioid withdrawal symptoms.

This theory suggests that these cortical excitatory brain pathways are overactive in heroin addiction and that reducing their activity would be therapeutic. Scientists are currently researching a medication called lamotrigene and related compounds called excitatory amino acid antagonists to see whether this potential treatment strategy really can work.

The excitatory cortical pathways may produce little response in the VTA during the resting state, leading to reductions in DA. However, when the addicted individual is exposed to cues that produce craving, the glutamate pathways may get sufficiently active to raise DA and stimulate desire for a greater high.

This same increase in glutamate activity will raise NA release from the LC to produce a dysphoric state predisposing to relapse and continued addiction. The cognitive deficits model of drug addiction proposes that individuals who develop addictive disorders have abnormalities in an area of the brain called the prefrontal cortex PFC.

The PFC is important for regulation of judgment, planning, and other executive functions. To help us overcome some of our impulses for immediate gratification in favor of more important or ultimately more rewarding long-term goals, the PFC sends inhibitory signals to the VTA DA neurons of the mesolimbic reward system.

The cognitive deficits model proposes that PFC signaling to the mesolimbic reward system is compromised in individuals with addictive disorders, and as a result they have reduced ability to use judgment to restrain their impulses and are predisposed to compulsive drug-taking behaviors. Consistent with this model, stimulant drugs such as methamphetamine appear to damage the specific brain circuit—the frontostriatal loop—that carries inhibitory signals from the PFC to the mesolimbic reward system.

In addition, a recent study using magnetic resonance spectroscopy showed that chronic alcohol abusers have abnormally low levels of gamma-amino butyric acid GABA , the neurochemical that the PFC uses to signal the reward system to release less DA Behar et al. As well, the cognitive deficits model of drug addiction could explain the clinical observation that heroin addiction is more severe in individuals with antisocial personality disorder—a condition that is independently associated with PFC deficits Raine et al.

In contrast to stimulants, heroin apparently dam-ages the PFC but not the frontostriatal loop. Therefore, individuals who become heroin addicts may have some PFC damage that is independent of their opioid abuse, either inherited genetically or caused by some other factor or event in their lives.

This preexisting PFC damage predisposes these individuals to impulsivity and lack of control, and the additional PFC damage from chronic repeated heroin abuse increases the severity of these problems Kosten, That drug abuse patients are more vulnerable to stress than the general population is a clinical truism. In the research arena, numerous studies have documented that physical stressors such as footshock or restraint stress and psychological stressors can cause animals to reinstate drug use and that stressors can trigger drug craving in addicted humans e.