No,no,no. I looked up this up extensively & unless they have tylonol in them the only & not proven effects of long term opiate use is cognitive effects. No liver damage no kidney damage. I've been on hardcore opiates for 10 years & my liver panel is just fine. Google it & read it.
From my personal experience - cognitive problems and memory loss, liver damage, severe motility and constipation problems (messes up your gut so much that nothing I take - prescription, herbal, etc helps anymore, and losing teeth due to decay from the dry mouth. Regards - ElizaJane
Often times, cognitive memory loss is BECAUSE of pain. There have been studies that with chronic long term pain, you lose white matter in the brain. Not that this can't be reversed, but the pain issue has to end also. Buddy is right, google it.
The following is from Wikipedia:
Common adverse reactions in patients taking opioids for pain relief include: nausea and vomiting, drowsiness, itching, dry mouth, miosis, and constipation.
Oxycodone and codeine may double mortality as compared to hydrocodone. In contrast to hydrocodone, oxycodone and codeine are metabolized by cytochrome P-450 CYP2D6 which may lead to variable pharmacokinetics due to single-nucleotide polymorphisms and drug interactions.
Infrequent adverse reactions in patients taking opioids for pain relief include: dose-related respiratory depression (especially with more potent opioids), confusion, hallucinations, delirium, urticaria, hypothermia, bradycardia/tachycardia, orthostatic hypotension, dizziness, headache, urinary retention, ureteric or biliary spasm, muscle rigidity, myoclonus (with high doses), and flushing (due to histamine release, except fentanyl and remifentanil).
Opioid-induced hyperalgesia has been observed in some patients, whereby individuals using opioids to relieve pain may paradoxically experience more pain as a result of their medication. This phenomenon, although uncommon, is seen in some palliative care patients, most often when dose is escalated rapidly. If encountered, rotation between several different opioid analgesics may mitigate the development of hyperalgesia.
Both therapeutic and chronic use of opioids can compromise the function of the immune system. Opioids decrease the proliferation of macrophage progenitor cells and lymphocytes, and affect cell differentiation (Roy & Loh, 1996). Opioids may also inhibit leukocyte migration. However the relevance of this in the context of pain relief is not known.
Men who are taking moderate to high doses of an opioid analgesic long-term are likely to have subnormal testosterone levels, which can lead to osteoporosis and decreased muscle strength if left untreated. Therefore, total and free testosterone levels should be monitored in these patients; if levels are suboptimal, testosterone replacement therapy, preferably with patches or transdermal preparations, should be given. Also, prostate-specific antigen levels should be monitored.
Use of opioids may be a risk factor for failing to return to work.
In addition, lack of employment may be a predictor of aberrant use of prescription opioids.
Opioids may increase risk of traffic accidents and accidental falls.
Managing adverse effects
Nausea: tolerance occurs within 7–10 days, during which antiemetics (e.g. low dose haloperidol once at night) are very effective. Due to severe side effects such as tardive dyskinesia, haloperidol is currently rarely used. A related drug, Compazine (prochlorperazine) is more often used, although it has similar risks. Stronger antiemetics such as ondansetron or tropisetron may be indicated if nausea is severe or continues for an extended period, although these tend to be avoided due to their high cost unless nausea is really problematic. A cheaper alternative is dopamine antagonists, e.g. domperidone and metoclopramide. Domperidone does not cross the blood–brain barrier, so blocks opioid emetic action in the chemoreceptor trigger zone without adverse central anti-dopaminergic effects (not available in the U.S.) Some antihistamines with anti-cholinergic properties (e.g. orphenadrine or diphenhydramine) may also be effective. The first-generation anti-histamine hydroxyzine is very commonly used, with the added advantages of not causing movement disorders, and also possessing analgesic-sparing properties.
5-HT3 antagonists (e.g. ondansetron)
Dopamine antagonists (e.g. domperidone)
Anti-cholinergic antihistamines (e.g. diphenhydramine)
Vomiting: this is due to gastric stasis (large volume vomiting, brief nausea relieved by vomiting, oesophageal reflux, epigastric fullness, early satiation), besides direct action on the vomiting centre of the brain. Vomiting can thus be prevented by prokinetic agents (e.g. domperidone or metoclopramide 10 mg every eight hours). If vomiting has already started, these drugs need to be administered by a non-oral route (e.g. subcutaneous for metoclopramide, rectally for domperidone).
Prokinetic agents (e.g. domperidone)
Anti-cholinergic agents (e.g. orphenadrine)
Drowsiness: tolerance usually develops over 5–7 days, but if troublesome, switching to an alternative opioid often helps. Certain opioids such as fentanyl, morphine and diamorphine (heroin) tend to be particularly sedating, while others such as oxycodone, tilidine and meperidine (pethidine) tend to produce comparatively less sedation, but individual patients responses can vary markedly and some degree of trial and error may be needed to find the most suitable drug for a particular patient. Treatment is at any rate possible - CNS stimulants are generally effective.
Stimulants (e.g. caffeine, modafinil, amphetamine, methylphenidate)
Itching: tends not to be a severe problem when opioids are used for pain relief, but if required then antihistamines are useful for counteracting itching. Non-sedating antihistamines such as fexofenadine are preferable so as to avoid increasing opioid induced drowsiness, although some sedating antihistamines such as orphenadrine may be helpful as they produce a synergistic analgesic effect which allows smaller doses of opioids to be used while still producing effective analgesia. For this reason some opioid/antihistamine combination products have been marketed, such as Meprozine (meperidine/promethazine) and Diconal (dipipanone/cyclizine), which may also have the added advantage of reducing nausea as well.
Antihistamines (e.g. fexofenadine)
Constipation: develops in many people on opioids and since tolerance to this problem does not develop readily, most patients on long-term opioids will need a laxative. Over 30 years experience in palliative care has shown that most opioid constipation can be successfully prevented: "Constipation … is treated [with laxatives and stool-softeners]" . According to Abse, "It is very important to watch out for constipation, which can be severe" and "can be a very considerable complication" if it is ignored. Peripherally acting opioid antagonists such as alvimopan (Entereg) and methylnaltrexone (Relistor) have been found to effectively relieve opioid induced constipation without triggering withdrawal symptoms, although alvimopan is contraindicated in patients who have taken opioids for more than seven days, is only FDA-approved for 15 doses or less, and may increase risk of heart attack. For mild cases, a lot of water (around 1.5 L/day) and fiber might suffice (in addition to the laxative and stool-softeners).
Stool-softening and peristalsis-promoting laxatives (e.g. docusate in combination with bisacodyl or senna).
Peripherally-acting opioid antagonists (e.g. methylnaltrexone) effectively prevent constipation while not affecting centrally mediated analgesia or provoking withdrawal syndrome, however these can still potentially reduce the efficacy of opioid analgesics in the treatment of conditions where much of the pain relief comes from action at peripherally situated opioid receptors, such as in inflammatory conditions like arthritis or post-surgical pain.
High water intake and dietary fiber
For more severe and/or chronic cases, the drugs that are used work by not increasing peristalsis, but by preventing water uptake in the intestine, leading to a softer stool with a larger component of water, and, additionally, by acidifying the environment inside the intestine, which both decreases water uptake and enhances peristalsis (e.g. lactulose, which is controversially noted as a possible probiotic). The following drugs are generally efficacious:
Polyethylene glycol 3350±10% dalton powder for solution (MiraLax, GlycoLax).
One combination, oxycodone/naloxone, aims to reduce systemic side effects by combining oxycodone with an opioid suppressor, naloxone, in a form which does not pass through the blood–brain barrier. Thus, the constipation effect is suppressed, but not the pain reduction.
Respiratory depression: although this is the most serious adverse reaction associated with opioid use it usually is seen with the use of a single, intravenous dose in an opioid-naïve patient. In patients taking opioids regularly for pain relief, tolerance to respiratory depression occurs rapidly, so that it is not a clinical problem. Several drugs have been developed which can partially block respiratory depression, although the only respiratory stimulant currently approved for this purpose is doxapram, which has only limited efficacy in this application. Newer drugs such as BIMU-8 and CX-546 may however be much more effective.
Respiratory stimulants: carotid chemoreceptor agonists (e.g. doxapram), 5-HT4 agonists (e.g. BIMU8), δ-opioid agonists (e.g. BW373U86) and AMPAkines (e.g. CX717) can all reduce respiratory depression caused by opioids without affecting analgesia, but most of these drugs are only moderately effective or have side effects which preclude use in humans. 5-HT1A agonists such as 8-OH-DPAT and repinotan also counteract opioid-induced respiratory depression, but at the same time reduce analgesia, which limits their usefulness for this application.
Opioid antagonists (e.g. naloxone, nalmefene, diprenorphine)
Hyperalgesia: side effects such as hyperalgesia and allodynia, sometimes accompanied by a worsening of neuropathic pain, may be consequences of long-term treatment with opioid analgesics, especially when increasing tolerance has resulted in loss of efficacy and consequent progressive dose escalation over time. This appears to largely be a result of actions of opioid drugs at targets other than the three classic opioid receptors, including the nociceptin receptor, sigma receptor and Toll-like receptor 4, and can be counteracted in animal models by antagonists at these targets such as Naloxone respectively. No drugs are currently approved specifically for counteracting opioid-induced hyperalgesia in humans and in severe cases the only solution may be to discontinue use of opioid analgesics and replace them with non-opioid analgesic drugs. However since individual sensitivity to the development of this side effect is highly dose dependent and may vary depending which opioid analgesic is used, many patients can avoid this side effect simply through dose reduction of the opioid drug (usually accompanied by addition of a supplemental non-opioid analgesic), rotating between different opioid drugs, or by switching to a milder opioid with mixed mode of action that also counteracts neuropathic pain, particularly tramadol or tapentadol.
NMDA antagonists such as ketamine
SNRIs such as milnacipran
anticonvulsants such as gabapentin or pregabalin
Finally, opioid effects (adverse or otherwise) can be reversed with an opioid antagonist such as naloxone or naltrexone. These competitive antagonists bind to the opioid receptors with higher affinity than agonists but do not activate the receptors. This displaces the agonist, attenuating and/or reversing the agonist effects. However, the elimination half-life of naloxone can be shorter than that of the opioid itself, so repeat dosing or continuous infusion may be required, or a longer acting antagonist such as nalmefene may be used. In patients taking opioids regularly it is essential that the opioid is only partially reversed to avoid a severe and distressing reaction of waking in excruciating pain. This is achieved by not giving a full dose but giving this in small doses until the respiratory rate has improved. An infusion is then started to keep the reversal at that level, while maintaining pain relief. Opioid antagonists remain the standard treatment for respiratory depression following opioid overdose, with naloxone being by far the most commonly used, although the longer acting antagonist nalmefene may be used for treating overdoses of long-acting opioids such as methadone, and diprenorphine is used for reversing the effects of extremely potent opioids used in veterinary medicine such as etorphine and carfentanil. However since opioid antagonists also block the beneficial effects of opioid analgesics, they are generally useful only for treating overdose, with use of opioid antagonists alongside opioid analgesics to reduce side effects, requiring careful dose titration and often being poorly effective at doses low enough to allow analgesia to be maintained.
This may be a bit more complicated an answer than you were looking for, but here it is spelled out for you. Best wishes to you!
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