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Nonopioid Analgesics
 

Two things that may keep patients from seeking dental care are pain and anxiety.

The sensation of pain is the means by which the body is made aware of the presence of damage or potential damage.

There are many different levels of pain perception among individuals.

The class of centrally acting analgesics are called opioids because they are opium like. They are also called narcotics.

The Nonnarcotic analgesics act principally, in terms of analgesia, at the peripheral nerve endings at the site of tissue damage.

Opioids have a higher ceiling of activity (efficacy). In other words, they are more efficacious for pain relief.

Since opioids are centrally acting, there are a number of side effects such as sleepiness, hallucinations, changes in judgment, and altered reaction time.

Opioids are more dangerous in terms of adverse reactions and drug interactions.

Opioids have much better pain relief.

All the modern upper to high level analgesics are combination drugs. With combination drugs, you get the best of both worlds because you have a centrally acting drug combined with a peripherally acting drug.

There are only 2 salicylates with medicinal value. These are aspirin and Dolobid.

Salicylates are peripherally acting agents.

Dolobid is almost always listed with NSAIDs, but it is actually a salicylate.

The very first NSAID was aspirin.

Aspirin, acetaminophen, and other peripherally acting agents are good for low to moderate pain. They are good for dull or throbbing pain and they are excellent for pain from inflammation. These drugs however, are ineffective against severe pain.

For severe pain, you must use an opioid drug

The combination of an opioid and a nonopioid analgesic in one drug makes a very effective drug. However, combining two nonopioids in one drug, such as aspirin and acetaminophen, is absolutely useless. You will not get an increase in efficacy by combining aspirin and acetaminophen.

Combining drugs with two different sites of action makes a very effective drug.

Nonopioid and opioid analgesics work at completely different sites by totally different mechanisms therefore; their combination in analgesic therapy makes very good sense because it provides much more complete relief from pain.

Aspirin is probably the most extensively prescribed analgesic, antipyretic, anticoagulant, and anti inflammatory agent.

Most common problem you will find with medications taken by mouth is GI irritation. This statement includes NSAIDs.

All the NSAIDs are nonspecific COX inhibitors.

COX – Cyclooxygenase (An enzyme responsible for the synthesis of prostaglandins)

By inhibiting COX (Cyclooxygenase), you inhibit the production of prostaglandins, therefore you inhibit pain.

All NSAIDs work by inhibiting prostonoid and prostaglandin synthesis and Cyclooxygenase.

NSAIDs also alleviate pain because they go to the hypothalamus and lower the temperature by inhibiting the prostonoid like substances in the hypothalamus.

The relief of pain occurs by inhibiting prostonoids at the peripheral tissues.

Lowering temperature occurs by inhibiting prostonoids in the hypothalamus.

Aspirin has some CNS activity, but only as an antipyretic.

Aspirin reduces fever by inducing peripheral vasodilatation and sweating.

In toxic doses, aspirin has the opposite effect. A toxic level can cause an anti-inflammatory, antithrombtic, and an adverse effect on the respiration. (severe respiratory depression).

The main difference of salicylate toxicity and acetaminophen toxicity:

Salicylate toxicity will manifest itself within minutes with difficulty in breathing, runny eyes, and runny nose. Acetaminophen toxicity takes about 7 days for symptoms to occur and it results in a much more serious condition called hepatic necrosis.

There is no known toxic dose for penicillin.

All pain relievers have toxic doses. 

Pharmacokinetics of Aspirin:

Aspirin is rapidly and almost completely absorbed from the stomach and small intestine. It reaches plasma concentrations and peak effect in 30 minutes – 1 hour. Aspirin has a good half life and is dosed about every 4 – 6 hours. The rate of absorption is determined by disintegration and dissolution rates of tablets, the pH at the mucosal surface, and gastric emptying times. This is true for everything you take by mouth. Aspirin is distributed through most body tissues and fluids. It readily passes through cell barriers and crosses the blood brain barrier very slowly. Aspirin is metabolized by the lever and follows first order kinetics. Aspirin is excreted primarily by the kidneys.

Buffering – raises the pH of the drug in order to avoid GI irritation. This doesn’t really work because this causes a greater degree of the ionized portion of the drug in the GI tract meaning there will be less absorption of the drug.

Entericaly coating a drug does not change the pH of the drug, it only allows the drug to withstand dissolution in the stomach, allowing it to get further down the GI tract to tougher tissue with less GI irritation potential.

People who take aspirin on a daily basis would benefit from an enterically coated aspirin.

Goody’s powders work really fast because the dissolution is not needed since it is in a powder form. One disadvantage of Goody’s powder and others like it is that they contain a lot of salt so it is not a good drug to use on a daily basis.

Doses:

Usual adult dose = 2 (5 grain tablets) This amounts to 650 mg every 4 – 6 hours.

On a log dose curve, a single dose of aspirin will have a linear increase in analgesia (efficacy) up to 1300 mg.

As you take greater amounts of aspirin, there is an increase in the chance of toxicity.

Alcohol increases the bleeding potential of aspirin.

Aspirin is considered a teratogenic drug.

An aspirin a day is recommended for patients with heart disease.

An aspirin every other day is recommended to lower your chance of colon cancer by 1/3.

Three types of people who may be more susceptible to aspirin toxicity are those with asthma, chronic urticaria, and nasal polyps.

An overdose of aspirin can cause urticaria, angioedema, bronchospasms, and severe runny nose within 3 hours.

All NSAIDs have the potential for GI irritation. 

P-aminophenols:

The only p-aminophenol that has any medicinal purpose is acetaminophen.

N-acetyl- paminophenol = Acetaminophen

Acetaminophen is very similar to aspirin. It is a very weak inhibitor of prostanoid biosynthesis; therefore, it has virtually no anti inflammatory effect. Because of this, it is not effective in the treatment of arthritis.

The peak concentration of Acetaminophen is 60 minutes.

The pain threshold is 30 minutes.

Acetaminophen has the same kind of dosing as aspirin.

Acetaminophen is nonteratogenic and can be used in pregnancy.

If high doses of acetaminophen is ingested, a toxic metabolite called N-acetyl-p-benzoquinonamine is produced, which causes hepatic necrosis.

The most serious adverse effect of acetaminophen is hepatic necrosis.

Hepatic toxicity can occur after the ingestion of a single dose of 10 – 15 g of acetaminophen.

Acetaminophen intolerance is very rare.

Acetaminophen is a good substitute for patients with aspirin hypersensitivity. 

Other NSAIDs

From a technical standpoint, you could almost classify aspirin as a NSAID, but it’s usually referred to as a salicylate.

NSAIDs were first used to treat arthritis and are now used for analgesia as well.

If you inhibit the arachadonic acid cascade, you will inhibit the enzymes that are responsible for the synthesis of prostaglandins. By inhibiting this cascade, you would inhibit pain.

Celebrax and Vioxx are the only two COX specific inhibitors on the market.

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