ch 6: drugs for pain control

What are the 2 major classes of analgesics?

Nonopioid analgesics and opioid analgesics.

Where do nonopioid analgesics act primarily?

At peripheral nerve endings; their antipyretic effect is mediated centrally.

Where do opioid analgesics act primarily?

In the central nervous system (CNS).

How do nonopioid analgesics generally reduce pain?

They inhibit prostaglandin synthesis.

How do opioids generally reduce pain?

They depress the CNS and alter the response/perception of pain.

What is nociceptive pain?

Pain arising from a stimulus or tissue injury outside the CNS.

What type of pain do A-delta fibers conduct?

Sharp, localized pain.

What type of pain do C fibers conduct?

Dull, poorly localized pain.

What is neuropathic pain?

Pain caused by a lesion or disease of the somatosensory nervous system.

What are cyclooxygenases (COX-1 and COX-2)?

Enzymes that catalyze formation of prostaglandins and thromboxane from arachidonic acid.

Why do NSAIDs work well for inflammatory dental pain?

They inhibit COX/prostaglandin production, reducing pain and inflammation.

What is the major role of COX-1?

Protective/housekeeping functions, including production of prostaglandins that protect GI epithelium and activation of platelets.

What is the major role of COX-2?

Associated primarily with inflammation and production of inflammatory prostaglandins.

Why can inhibition of COX-1 cause GI problems?

COX-1 helps produce prostaglandins that protect the stomach/GI epithelium; inhibition decreases this protection.

What does aspirin do to platelets?

Irreversibly inhibits platelet aggregation for the lifespan of the platelet, about 7–10 days.

What are the major actions of aspirin?

Antipyretic, antiplatelet, analgesic, anti-inflammatory, and uricosuric at high doses.

What is the purpose of low-dose 81 mg aspirin?

Helps protect against heart attack and stroke by reducing platelet aggregation.

What is the ceiling effect of aspirin?

After a certain dose, increasing the dose does not produce additional analgesic/anti-inflammatory benefit.

What does NSAID stand for?

Nonsteroidal anti-inflammatory drug.

How do most NSAIDs work?

Inhibit COX-1 and/or COX-2 → inhibit prostaglandin synthesis.

What are the major therapeutic effects of NSAIDs?

Analgesic, anti-inflammatory, and antipyretic effects.

What is a major adverse effect of NSAIDs?

GI bleeding.

What are common examples of NSAIDs?

Aspirin, ibuprofen, and naproxen.

What COX enzymes does ibuprofen inhibit?

COX-1 and COX-2.

What is a major adverse effect of ibuprofen?

Increased risk of GI bleeding.

What is the maximum daily dose of ibuprofen listed in the PowerPoint?

3200 mg/day.

What is celecoxib (Celebrex)?

A selective COX-2 inhibitor.

Why was celecoxib developed?

To reduce inflammation while avoiding the gastric effects associated with blocking COX-1.

What major warning is associated with celecoxib in the PowerPoint?

Increased risk of clotting and heart attack.

What are the 2 major therapeutic effects of acetaminophen?

Analgesic and antipyretic.

Is acetaminophen anti-inflammatory?

No.

How does acetaminophen differ from NSAIDs?

It provides analgesic and antipyretic effects but does not have significant anti-inflammatory or antiplatelet effects like NSAIDs.

What is another abbreviation/name for acetaminophen?

APAP (acetyl para-aminophenol); also called paracetamol.

What maximum safe acetaminophen dose is listed in the PowerPoint?

4000 mg/day, although the Tylenol manufacturer decreased its recommended maximum to 3000 mg/day.

Why is total daily acetaminophen exposure important?

Excessive doses can cause severe hepatotoxicity/acute liver failure.

Why can accidental acetaminophen overdose occur with combination medications?

Patients may take multiple products containing APAP without realizing their total daily dose.

What organ is primarily at risk from acetaminophen toxicity?

Liver.

What should chronic alcohol users be cautious about with acetaminophen?

Overuse because of increased risk of liver toxicity.

How do opioids work?

Bind opioid receptors in the CNS and spinal cord to alter the perception of pain.

What severity of pain are opioids generally used for?

Moderate to severe pain.

What are the 3 important opioid receptors listed?

Mu (μ), kappa (κ), and delta (δ).

What opioid receptors does morphine act on according to the PowerPoint?

Mu and kappa receptors.

What is naloxone (Narcan)?

An opioid antagonist that blocks opioid receptors.

What are major adverse effects/actions of opioids?

Nausea, miosis, constipation, histamine release/itching, euphoria, CNS depression, and respiratory depression.

What is the classic pupil finding with opioid use?

Miosis (pupil constriction).

What is the most serious major adverse effect of opioids?

CNS/respiratory depression.

Why are opioids dangerous when combined with other CNS depressants?

Their CNS/respiratory depressant effects can be additive, increasing the risk of severe respiratory depression.

What is physical dependence?

Physiologic adaptation to a drug in which stopping it can produce withdrawal.

Is physical dependence the same thing as addiction?

No; physical dependence is a physiologic adaptation, whereas addiction involves compulsive/problematic drug use.

Why are nonopioid analgesics especially useful for acute inflammatory dental pain?

Dental pain is often inflammatory, so reducing prostaglandin production directly targets an important source of the pain.