drugs used in dentistry

[dr.amr]

Drugs Used in Dentistry

ANALGESICS

Pain Control
Pain, as defined by the International Association for the Study of Pain, is "an unpleasant sensory and emotional experience arising from actual or potential tissue damage or described in terms of such damage." It is often pain that brings the patient to the dental office. Conversely, fear of pain is a significant reason for many people to avoid seeking dental care. No matter how successful or how deftly conducted, most dental procedures produce tissue trauma and release potent mediators of inflammation and pain. We now know that unrelieved pain after surgery or trauma has negative physical and psychologic consequences.
The two components of pain are perception and reaction. Perception is the physical component of pain and involves the message of pain that is carried through the nerves eventually to the cortex. Reaction is the psychological component of pain and involves the patient's emotional response to the pain. Although individuals are surprisingly uniform in their perception of pain, they vary greatly in their reaction to it. A decrease in the pain threshold (a greater reaction to pain) has been associated with emotional instability, anxiety, fatigue, youth, certain nationalities, women, and fear and apprehension. The pain threshold is raised by sleep, sympathy, activities, and analgesics.
Fortunately, pain is preventable or controllable in an overwhelming majority of cases. Patients have a right to treatment that includes prevention of pain and adequate relief of pain.
Undertreatment of pain is a significant problem. Numerous clinical surveys have shown that postoperative pain is often inadequately treated because of undermedication, leaving patients to suffer needlessly.
Successful assessment and control of pain depend, in part, on establishing effective communication between the dentist and the patient. Patients should be informed that pain relief is an important part of their health care. Pain is a subjective phenomenon. The patient's self-report is the single most accurate and reliable indicator of the existence and intensity of pain and any resultant distress. Pain is whatever the experiencing person says it is and exists whenever he says it does.
A significant barrier to the effective use of analgesics in managing pain involves several misconceptions regarding pain and its control held by both patients and health care providers.

Misconception 1_Patients who are in pain always have
observable signs. Although many patients in acute pain exhibit evidence of anxiety, distress, or decreased function, many do not.

Misconception 2_Obvious pathology, test results, and/or the type
of surgery determine the existence and the intensity of pain. Although the ability to identify a pathologic process underlying a patient's pain complaint is a key element in planning and initiating definitive treatment, failure to identify the source of a patient's pain does not necessarily mean than it does not exist.

Misconception 3_Patients should wait as long as possible before taking a pain medication. This abstinence will teach them to have a better tolerance for pain. Pain that is untreated often escalates. Without treatment, sensory input from injured tissue reaches spinal cord neutrons and causes subsequent responses to be enhanced. Aggressive pain prevention and control that occurs before, during, and after a painful event such as dental surgery can yield both short- and long-term benefits. Patients should be encouraged to use analgesics before pain becomes severe and difficult to control.

The most common types of odontogenic pain are characterized
as acute pain. Characteristically, acute pain is accompanied by some recognizable evidence of tissue injury or inflammation, and it resolves spontaneously once the underlying cause (inflamed pulp, abscessed tooth, carious lesion) is definitively treated. Few underlying psychologic or behavioral issues affect the dentist's choice of therapies, and, most commonly, a pharmacologic approach to pain management is most appropriate.
In contrast, management of chronic facial pain involves much more complex treatment issues. Chronic pain often lasts months or years beyond the precipitating event, and there is rarely a readily identifiable source, that is, an area of tissue destruction or inflammation. There is often a complicated set of behavioral issues that must be explored and clarified. Pharmacologic approaches to chronic pain are rarely the sole or principal means of managing these disorders.

Peripherally acting analgesics reduce or control pain by directly
inhibiting the biochemical mediators of pain at the site of injury. In addition to their analgesic property, the majority of drugs in this class have antiinflammatory and antipyretic activity. In fact, they are often referred to as the NSAIDs or antipyretic analgesics.
Opioids on the other hand, decrease the perception of pain in the CNS. The opioid analgesics act in the CNS at receptors in the spinal cord, rostroventral medulla, and periaqueductal gray matter. These anatomic loci are considered important to the perception of pain.

Analgesic Agents

Analgesic agents can be divided into two groups: the nonopioid, nonnarcotic and the opioid narcotic. An important difference between the nonopioid and the opioid analgesics is their site of action. Nonopioid analgesics act primarily at the peripheral nerve endings, although they also act centrally. Opioids act within the central nervous system.
Another difference between the opioids and the nonopioid analgesic agents is their mechanism of action. The action of the nonopioid analgesic agents is related to their ability to inhibit prostaglandin synthesis. The opioids affect the amount of pain by depressing the CNS (the reaction).

Nonsteroidal antiinflammatory drugs (NSAIDs) act at the site of
initiation of noxious impulses. Although it is difficult to separate their antiinflammatory effects from their analgesic effects, nonopioid drugs such as the salicylates and other NSAIDs work predominantly in the periphery by preventing the synthesis and release of inflammatory mediators that sensitize noninceptive receptors to other
algesic mediators, such as bradykinin, and to physical forces.

Recent studies suggest that NSAIDs may also have central
effects. Acetaminophen has been shown to have analgesic and antipyretic properties, but it lacks significant antiinflammatory effects. Acetaminophen appears to exert its effects both in the CNS and in the periphery.

The peripherally acting or antipyretic analgesics comprise various chemical classes of drugs that have a similar mechanism of action and share clinically important analgesic, antiinflammatory, and antipyretic properties. These analgesics are widely prescribed by dentists and physicians because they can be taken orally, they do not cause central nervous system (CNS) or respiratory depression at therapeutic doses (as do the centrally acting opioid analgesics), and, most important, they are
very effective pain relievers
.
Aspirin and acetaminophen have been recognized for many years as prototypes for the peripherally acting analgesics. Today, the propionic acid derivatives, led by ibuprofen, have successfully challenged the clinical status of these older drugs and have established a new standard for comparison. Some of the claims made for these agents are greater peak analgesia, longer durations of action, and a lower incidence of side effects. Because the dentist must treat acute pain on a daily basis, the peripherally acting analgesics are of particular importance.
Nonopioid Analgesics

This category comprises various groups of drugs that have a similar mechanism of action and share clinically important analgesic, antiinflammatory, and antipyretic properties. These agents differ from opioid analgesics in the following ways: (1) there is a ceiling effect to the analgesia; (2) they do not product tolerance or physical dependence; (3) they are antipyretic; and (4) they possess both antiinflammatory as well as analgesic properties, except for acetaminophen, which has minimal antiinflammatory activity. Pharmacologic management of mild to moderate pain should begin, unless there is a contraindication, with a nonopioid drug such as acetaminophen, a salicylate, or another NSAID. As a general rule, any analgesic regimen should include a nonopioid drug, even if pain is severe enough to require
the addition of an opioid
.
Nonopioids are most effective in treating postprocedural pain
when given before the procedure ( or immediately following a short procedure), thus preventing the synthesis of prostaglandins that quickly follow the surgical insult. The delayed use of NSAIDs post-procedurally inhibits the subsequent prostaglandin synthesis and provides analgesia, but it does not interfere with the effects of those prostaglandins already produced. Preoperative administration of NSAIDs delays the onset of postoperative pain and lessens its severity and subsequent analgesics requirements
.
The NSAIDs all share a qualitatively similar side-effect profile. However, with the exception of a true allergic reaction and the bronchoconstriction response in asthmatics, a patient's inability to tolerate one specific NSAID does not mean the patient will be intolerant of all other NSAIDs. Also, patients may vary in their relative analgesics response to various NSAIDs. Therefore, if a patient does not respond to a particular drug at the maximum therapeutic dose, an alternative NSAID should be considered.

The oral route of administration is preferred for nonopioids. Some
patients, such as young children or patients with intermaxillary fixation following maxillofacial surgery or trauma, are unable to swallow tablets or capsules. For these patients, liquid formulations of acetaminophen or ibuprofen should be considered. For the rare dental patient who is unable to take any medications by mouth, parenteral (ketorolac) or rectal (acetaminophen, aspirin) dosage forms are available.
The nonopioids can be divided into the salicylates (aspirin-like group), acetaminophen, and the nonsteroidal anti-inflammatory
agents or drugs (NSAIAs/NSAIDs).

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[Dr. Do0o0ody]

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وجزاااك الله خير

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The inhibition of prostaglandin synthesis produced by aspirin is also responsible for its antiinflammatory action, a primary objective in dental pain relief. The prostaglandins are important vasodilating agents that also increase capillary permeability. Therefore, aspirin causes decreased erythema and swelling of the inflamed area.

Aspirin and Related Salicylates
Aspirin has been commercially available since 1899, and, until the late 1970s, no peripherally acting analgesics could claim greater efficacy.
Aspirin belongs to the salicylic acid (salicylate) class of compounds that were originally obtained from botanical sources. The first active substance of this group, salicin, was isolated from the bark of the willow tree. From salicin were synthesized salicylic acid, sodium salicylate, and finally acetylsalicylic acid (aspirin).
Aspirin, the most prominent member of the salicylate group, derives its analgesic, antipyretic, and antiinflammatory action from its ability to inhibit prostaglandin systhesis. Aspirin inhibits the enzyme cyclooxygenase (prostaglandin synthase) by acetylating a serine, which results in inhibition of the production of prostaglandins. A reduction in prostaglandins results in a reduction in painful perception. Many dental patients are advised to take aspirin before the painful stimuli is experienced, such as a "throbbing" pain caused by inflammation.

The antipyretic properties of aspirin are well documented. Antipyresis is best demonstrated in febrile patients, since normal subjects show no marked change in body temperature when therapeutic doses of aspirin are administered.
It is difficult to separate the analgesic and antiinflammatory effects of aspirin, since the vast majority of painful conditions have an inflammatory component. There is little doubt that the cascade of reactions leading to the formation of prostaglandins is integrally involved with the inflammatory response and that aspirin's efficacy in treating inflammation is closely related to its inhibition of prostaglandin synthesis.

Aspirin is rapidly and almost completely absorbed from the stomach and small intestine, producing a peak effect on an empty stomach in 30 minutes. The buffered tablet reaches its peak in about 50 minutes. Addition of a buffer to aspirin facilitates the dispersion and dissolution of the tablet.
Aspirin may be administered rectally when vomiting is present. Since this route is more erratic and unpredictable it should only be used when the oral route is not feasible. An aspirin tablet should never be applied topically to the oral mucosa to treat a toothache. A painful ulceration can occur.
Aspirin is typically used to relieve mild to moderate pain such as a headache or toothache. It is not effective against intense pain because the analgesic potency of aspirin is weaker than that of the opioids.

Aspirin has been reported to have three kinds of adverse effects on the gastrointestinal system. The first is gastric distress. There is evidence suggesting that both local and systemic mechanisms interfere with the ability of gastric mucosal cells to resist penetration by acid. Aspirin's interference with normal cytoprotective mechanisms mediated by prostaglandins in gastric mucosal cells is a primary cause of the gastric distress. A second effect of aspirin is occult gastric bleeding, resulting from cellular and capillary damage along the gastrointestinal tract. The third effect, which is very rare and idiosyncratic, is a sudden acute hemorrhage.

Aspirin significantly increases bleeding time by inhibiting the aggregation of platelets. As little as one 325 mg aspirin tablet can double the normal bleeding time for several days. This protracted inhibition of platelet aggregation correlates with the ability of aspirin to irreversibly acetylate cyclooxygenase. Platelets lack the ability to regenerate this enzyme, and the synthesis of new platelets is required for recovery to occur.
Aspirin in dentistry Aspirin is an effective analgesic for almost any type of acute dental pain. Double-blind, controlled studies of the relief of pain after extraction of third molars have demonstrated that 650 mg of aspirin is substantially more effective than 60 mg of codeine in relieving postoperative pain. In fact, most controlled clinical studies have established that, regardless of the cause of the pain, aspirin (650 mg) provides equal or greater pain relief than codeine (60 mg). A problem with aspirin is that it has a rather flat dose-response curve, with near-maximal analgesia occurring at approximately 650 mg. Increasing the dose to 1000 mg may slightly increase analgesic efficacy and prolong the duration of effect. Clinically, this means that if 650 to 1000 mg of aspirin fails to relieve the discomfort, increasing the dose will be of little help. However, it cannot be overemphasized that at this ceiling dosage, taken every 4 hours, aspirin is a very effective analgesic for most painful dental conditions.


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Adverse effects Aspirin has numerous side effects at therapeutic doses, most of which are more annoying than serious. The most commonly reported side effect is nausea. It is important to realize that many surgical procedures or illnesses may cause nausea by themselves and that the analgesic may be blamed unjustly.
Certainly, many dental surgical procedures have the potential for causing nausea because of the swallowing of blood and debris, the use of sedative or anesthetic drugs, and the anxiety associated with dental surgery. However, it is also clear that aspirin can cause gastric irritation that leads to nausea and, occasionally, vomiting. In addition to the effects of aspirin on the gastric mucosa, aspirin causes local irritation directly while the tablet is disintegrating and in contact with the gastric tissues.
The same mechanisms that produce nausea are probably involved in the occult bleeding that develops in over 70% of those who use the drug. This blood loss occurs each time aspirin is ingested, occurs even at low doses, and goes unnoticed unless stool tests for blood are performed. Only in very unusual circumstances is this occult bleeding, which amount to less than 10 mL/day, of any clinical significance. However, aspirin is contraindicated in patients with gastrointestinal ulcers, especially those with peptic ulcers, because the normally innocuous bleeding may lead to severe internal hemorrhaging.
Aspirin significantly increases bleeding time by inhibiting the aggregation of platelets. Although the prolongation of clotting time is tolerated in healthy patients, the possibility exists that aspirin could promote postoperative hemorrhaging, especially if a clot has not fully formed. In two studies of patients undergoing dental impaction surgery, the administration of analgesic doses of aspirin was associated with significantly more postoperative swelling than comparable doses of acetaminophen. In view of these experimental findings, it may be prudent to recommend that aspirin therapy be discontinued before surgical procedures such as tooth extraction and that aspirin not be used prophylactically before any procedure that may involve postoperative bleeding. However, once a clot has been established, there should be little problem caused by the administration of aspirin or related salicylates.
Toxicity caused by aspirin overdose is common. Its symptoms and severity depend on dose. Chronic toxicity caused by salicylates is called salicylism and is characterized by tinnitus, nausea, vomiting, headache, hyperventilation, and mental confusion. Aspirin holds the dubious distinction of being one of the more frequently used drugs for attempted suicides.
The hyperventilation eventually can lead to respiratory alkalosis, which may be followed by a combined respiratory and metabolic acidosis accompanied by dehydration. Acidosis is more prominent as the level of overdose increases. Acidosis is also more likely to occur in children and infants. Impaired vision, hallucinations, delirium, and other CNS effects may be evident, and the situation is considered life threatening.
The treatment of aspirin overdose is primarily palliative and supportive. Chronic toxicity usually only requires removal of the drug and eventual dose adjustment. Acute toxicity often requires respiratory support, gastric lavage, maintenance of electrolyte balance (e.g., potassium replacement if necessary), maintenance of plasma pH, and alkalinization of the urine by intravenous (IV) bicarbonate.
Intolerance to salicylates can occur, with symptoms ranging from rhinitis to severe asthma. The reaction is more common in patients with preexisting asthma or nasal polyps. This does not appear to be an immune-mediated reaction. Intolerance occurs to other NSAIDs as well. The incidence of this kind of reaction in asthmatic patients has been reported to be as high as 20%. Patients with a history of asthma, allergic disorders, or nasal polyps should be questioned to be sure that they can tolerate aspirin.
Aspirin is contraindicated in a number of medical conditions. Serious internal bleeding can result from the ingestion of aspirin by a patient with an ulcer condition.
Aspirin is not contraindicated in pregnancy, but it should be used with caution. In the third trimester, aspirin tends to prolong labor by inhibiting the synthesis of prostaglandins involved in initiating uterine contractions. Aspirin has also been reported to increase blood loss at the time of delivery and may cause premature closure of the ductus arteriosus in the fetus. Aspirin should also be avoided in children with influenza or chickenpox (varicella). There are epidemiologic data indicating that aspirin usage during or shortly after these viral diseases increases the risk of developing Reye's syndrome.

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Acetaminophen
Acetaminophen is the only aniline derivative currently in clinical use. It is widely promoted as the antipyretic analgesic of choice when aspirin cannot be used because of gastric problems or other contraindications.
Acetaminophen has both analgesic and antipyretic activity that is essentially equivalent to that of aspirin. Acetaminophen's mechanism of action also appears to be the same as that of aspirin.
Compared with aspirin, acetaminophen has relatively few important effects on specific organs or systems. The potency and efficacy of acetaminophen as an antipyretic are similar to those of aspirin. At therapeutic doses, acetaminophen has little, if any, effect on the cardiovascular or respiratory systems.

Acetaminophen does not inhibit platelet aggregation, cause occult bleeding or gastric irritation, affect uric acid excretion, or have as many drug interactions as aspirin. In overdose, the organ most affected is the liver. Acute renal toxicity may also occur.
The wide publicity given to the adverse effects of aspirin has caused increasing numbers of dentists to substitute acetaminophen for aspirin in the treatment of postoperative dental pain, even though the antiinflammatory effects of acetaminophen are minor. In clinical studies, aspirin and acetaminophen appear to be similar in their effectiveness in relieving pain after the extraction of third molars.
Until recently, acetaminophen was thought to have a plateau for analgesia at about 650 mg, but it is now accepted that acetaminophen does have a linear dose-effect curve for analgesia up to 1000 mg. Based on this finding, some clinicians are recommending the use of 1000 mg of acetaminophen rather than the customary 650 mg dose.
The potential for adverse effects from acetaminophen seems to be singularly confined to the situation in which there is an acute overdose. At therapeutic doses, acetaminophen does not cause nausea, inhibit platelet aggregation, prolong prothrombin time, or produce the other side effects associated with the use of aspirin. Allergy to acetaminophen is rare and is generally manifested as skin eruptions.

Analgesic Alternatives to Aspirin and Acetaminophen
Until the late 1970s, no single-entity oral analgesic had consistently demonstrated grater analgesic efficacy than that of aspirin or acetaminophen. Several new peripherally acting analgesics, most of which had earlier been approved for use as antiinflammatory drugs, have now been evaluated in postoperative dental pain and found to be superior to the standard drugs in peak analgesic effect, duration of effect, or both.

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Among the NSAIDs, the propionic acid derivatives constitute the largest group of aspirin alternatives. Ibuprofen, fenoprofen, ketoprofen, and naproxen are approved for use as analgesics. Others, such as flurbiprofen, are currently under review by the Food and Drug Administration (FDA).

Ibuprofen was the first single-entity oral analgesic to be approved by the FDA that showed a greater peak effect than 650 mg. of aspirin. It is also available as a nonprescription drug. The recommended prescription analgesic dose of ibuprofen is 400 mg every 5 to 6 hours. In one study, this dose was more effective than a combination of 650 mg aspirin with 60 mg codeine.

Naproxen is approved for a variety of inflammatory conditions and for the relief of pain. It is available as both the free acid and as the sodium salt, the latter of which is more rapidly absorbed from the gastrointestinal tract and may be preferred form for analgesic use. The recommended analgesic regimen for naproxen is 500 mg initially, followed by 250 mg every 6 to 8 hours. Its longer half-life allows dosing at longer intervals than with ibuprofen.

Fenoprofen is marketed with both analgesic and antiinflammatory indications. The recommended dose of 200 mg every 4 to 6 hours is likely to be superior to 650 mg of aspirin.
Adverse effects The adverse effects of the peripherally acting analgesics are similar to those produced by aspirin; however, they may vary in severity. Gastric irritation (nausea and abdominal pain) is usually the most troublesome adverse effect. Dizziness, gastrointestinal bleeding, fluid retention, and nephrotoxicity have also been reported. Inhibition of platelet aggregation is transient and reversible.

These peripherally acting analgesics should be avoided in most patients whose medical conditions contraindicate the use of aspirin. Of particular concern are patients with gastrointestinal ulcers, coagulation disorders, and aspirin intolerance.

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Opioid Analgesics
Opioid analgesics are primarily employed for the relief of pain and consequently find widespread application in dentistry. Opioids also possess therapeutically useful antitussive (cough suppressant) and constipating effects in addition to several undesirable effects, including respiratory depression, urinary retention, sedation, nausea and vomiting, and at times unwanted constipation. Repeated use of opioids for control of pain can lead to analgesic tolerance (loss of analgesic effect), as well as physical and sometimes psychologic dependence. These shortcomings notwithstanding, no other drugs are more efficacious as analgesics than the opioids.

Opioid analgesics are added to nonopioids to manage pain that is moderate to severe or that does not respond to nonopioids alone. Opioids differ from the nonopioids in that they have no ceiling effect. The only dosing limitation is based on side effects. Although opioids are the cornerstone for management of moderate to severe acute pain, they are frequently underutilized and at lower than effective doses as a result of misconceptions and fears regarding their use.

Fear of possible sedation or respiratory depression causes some practitioners to underprescribe and underdose opioids. These adverse events rarely occur when appropriate starting doses are used and then titrated to an effect based on the patient's analgesic response and side effects. Patients vary greatly in their analgesic dose requirements and responses to opioid analgesics.

Fear of addiction on the part of both the practitioner and the patient is a common barrier to the effective use of opioid analgesics. For many, this fear is the result of not being aware of the actual risks associated with opioid analgesics used for the treatment of pain and of confusing addiction with physical dependence, tolerance, or pseudoaddiction. Addiction refers to psychologic dependence, a behavioral pattern of drug use marked by craving, drug-seeking behavior, and compulsive use that may interfere with the person's ability to function in society. Physical dependence, on the other hand, is a pharmacologic property causing the appearance of withdrawal symptoms when the medication is stopped abruptly or following the administration of an antagonist, and tolerance is the requirement for increased doses of a drug to achieve the same effect. Finally, pseudoaddiction is a term used to describe exaggerated behaviors seen in pain patients brought on by inadequate pain relief.

Physical dependence and tolerance are involuntary mechanisms that occur in virtually all patients taking opioid analgesics for a prolonged period of time. They are easily managed in the patient with pain. Tolerance is managed with careful upward titration of the dose until adequate pain relief is reobtained. The effects of physical dependence are easily avoided by the gradual tapering of opioids on discontinuation of therapy, as opposed to abrupt withdrawal. Addiction, by contrast, is a voluntary mechanism that rarely occurs in patients taking opioid analgesics for pain. The overwhelming majority of patients taking pain medication stop taking the medication when the pain stops.
Opioid analgesics include both pure agonists, such as codeine and oxycodone, and agonist/antagonists, such as pentazocine and butorphanol. As a general rule, the agonist/antagonists should not be used as first-line therapy. There is no convincing evidence that these drugs offer any advantage over the pure opioid agonists. Agonist/antagonists become less effective at high doses because of the ceiling effect, frequently cause dysphoria, and may cause confusion and hallucinations. In addition, they may cause withdrawal symptoms when given to patients physically dependent on opioid agonists. On occasion, they may be useful in treating individuals unable to tolerate other opioids.

In 1990, the World Health Organization proposed a stepwise approach for the management of cancer pain. This approach has subsequently come to be recommended for the treatment of noncancer pain as well. The first step, representing mild pain, is to administer a nonopioid drug. In many dental surgical procedures,

NSAIDs alone can achieve excellent pain control. Pain that does not respond adequately to nonopioid agents should be treated with the combination of a nonopioid and an opioid such as codeine, hydrocodone, or oxycodone. Even when insufficient alone to control pain, NSAIDs can reduce the dose of opioid relief. More severe pain, or pain that persists, should be treated with a combination of a nonopioid and a stronger opioid, such as morphine or hydromorphone. At any level, adjuvant agents such as certain anticonvulsants or tricyclic antidepressants may be added when indicated. Common indications in dentistry include the treatment of neuropathic pain and some chronic orofacial pain conditions.
The oral administration of opioid analgesics is preferred whenever possible. It is convenient and inexpensive. Even severe postsurgical pain can be effectively treated with orally administered opioids in the proper doses. For the patient not able to swallow a pill or capsule, numerous liquid formulations of opioids are available (codeine, hydrocodone, oxycodone, and others). Peak drug effects (including side effects) occur 1.5 to 2 hours after the oral administration of most opioids (sustained-release tablets excepted). Therefore, patients may take a second opioid dose safely 2 hours after the first dose if the pain persists and side effects are mild at that time. For patients unable to take medications by mouth, the intravenous, intramuscular, or rectal routes of administration can be considered. Use of the intravenous or intramuscular route to deliver analgesics is almost exclusively limited to inpatient hospital settings. Of the two routes, intravenous administration is preferred. Intravenous bolus administration provides the most rapid and predictable onset of effect. Time to peak effect varies with drug lipid solubility, ranging from 1 to 5 minutes for fentanyl to 15 to 30 minutes for morphine.
As mentioned previously, opioids should almost always be administered with nonopioids for maximum pain relief in dental situations. Many opioids are marketed in combinations with a nonopioid, and it is the latter component that limits the dose. For example, the upper dose limit for acetaminophen is 4000 mg/day. Therefore, for combinations containing 325 mg of acetominophen, the maximum number of tablets/day is 12. For combinations containing 500 mg of acetaminophen, the maximum number of tablets/day is eight. In children under 45 kg, the limit is 90 mg/kg of acetaminophen.

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Morphine
Morphine is the prototypic opioid analgesic and the one about which most is known. Morphine is widely used for pain control and can be given by virtually any route of administration.
The CNS effects of morphine are a combination of stimulation and depression and include analgesia, drowsiness, euphoria-dysphoria, respiratory depression, suppression of the cough reflex and pupillary constriction.

The analgesia produced by morphine and its congeners occurs without loss of consciousness. When opioids are administered for relief of pain (or for a cough or diarrhea, for that matter), it must be appreciated that they provide only symptomatic relief without alleviation of the cause of the pain (or cough or diarrhea). The analgesia produced by opioid analgesics is dose dependent and selective in that other sensory modalities (e.g., vision, audition) are unaffected at therapeutic doses. The standard parenteral analgesic dose of morphine, 10 mg/70 kg body weight, is considered a therapeutic dose for relief to severe pain. Greater doses provide greater pain control.

An additional significant feature of opioid analgesics is that they are generally more effective against continous, dull aching pain than against sharp, intermittent pain. Neuropathic pain, such as trigeminal neuralgia, is less responsive to opioids than is nociceptive pain. It is also known that sensitivity to pain and the ability to clear morphine decrease with age, whereas the elimination half-life of morphine does the opposite; thus, the pain relief provided by morphine typically increases with age.
Tolerance and dependence. Tolerance is a decreased effect of drug as a consequence of prior administration of that drug. Accordingly, increasingly greater dose of drug must be administered over time to produce an effect equivalent to that produced on initial administration. Tolerance does not develop uniformly to all opioid effects. In general, tolerance develops to the depressant effects of opioids but not to the stimulant effects. Thus, tolerance develops to opioid-induced analgesia, euphoria, drowsiness, and respiratory depression but not, to any appreciable extent, to opioid effects on the gastrointestinal tract or the pupil.

In the therapeutic setting, the initial indication that tolerance has developed is generally reflected in a shortened duration or reduced analgesic effect. The rate at which tolerance develops is function of the dose and the frequency of administration, as well as perhaps other, nonpharmacologic factors. In general, the greater the opioid dose and the shorter the interval between doses, the more rapid is the development of tolerance. Tolerance, in fact, can develop to such an extent that the lethal dose of the opioid is increased significantly. However, for any individual there always exists an opioid dose capable of producing death by respiratory depression regardless of the extent to which tolerance has developed.

Tolerance becomes apparent during repeated drug administration, whereas dependence is apparent only in the absence of drug. Dependence can be physical or psychologic state produced by repeated administration of a drug, which then makes its continued use necessary to prevent the appearance of a withdrawal or abstinence syndrome. The greater the opioid dose and the longer the duration of administration, the greater is the degree of physical dependence and the more intense is the withdrawal syndrome.

Psychologic dependence is more difficult to define and measure. Psychologic dependence contributes more to drug-seeking behavior than does physical dependence. Addiction is the extreme of compulsive drug use and is associated with significant psychologic dependence, and thus, it is inappropriate to identify as "addicted" a person who becomes physically dependent after repeated opioid administration during hospitalization. All three phenomena_tolerance, physical dependence, and psychologic dependence_are reversible, although psychologic dependence provides a strong drive to drug abuse.

There exists on the part of health professionals and patients alike concern about the use of opioids for pain control, particularly in cases of persistent pain. This so-called "opiophobia" is a reaction to fear of dose escalation (caused by development of tolerance) and subsequent physical dependence (erroneously termed "addiction") associated with treatment for pain that lasts more than a few days. It has been found, for example, that dose escalation for pain control is usually required only at the start of therapy (i.e., when titrating the dose to provide adequate analgesia) and that dose requirements tend to stabilize thereafter for long periods of time.

Pain is the main complaint that initiates a visit to a dentist or physician. Moreover, pain is almost always present after invasive procedures or surgery. Morphine and other opioid analgesics are the most efficacious analgesic drugs known and are without peer in their ability to control pain. As emphasized earlier, these drugs provide only symptomatic relief of pain without influencing its underlying cause. The opioids, when administered at therapeutic doses to produce analgesia, also produce a drowsiness from which the patient is generally easily aroused, as well as "tranquillization." There is without doubt a significant antianxiety or sedating component in the analgesic effect of opioids. Thus, although nausea and vomiting, respiratory depression, constipation, and tolerance and physical dependence can be drawbacks to their use, the opioids undeniably produce an important combination of desirable effects (e.g., analgesia and sedation) in the suffering patient.