Analgesics and Pain Classification

Pain caused by activation of nociceptors due to tissue damage, not nerve damage. This type of pain involves a functional somatosensory nervous system.

Pain originating from cancer or its treatment.

Pain not related to cancer or its treatment.

Short-term pain usually lasting less than 3 months.

Drugs that relieve pain.

Drugs that act on opioid receptors in the brain to relieve pain.

Drugs that block the effects of opioids.

Drugs that act on the 5-HT receptor to relieve pain, particularly migraines.

Acetaminophen's effects are diminished in the presence of high lipid hydroperoxides because these molecules oxidize the heme back to its active state, rendering acetaminophen ineffective.

Lipid hydroperoxides, particularly inflammatory HETEs, are molecules that oxidize heme, causing a decrease in acetaminophen's effectiveness.

Acetaminophen effectively inhibits prostanoid synthesis in cells with low basal peroxide tone.

Acetaminophen is ineffective in tissues with high peroxide tone, such as inflammatory conditions.

The effectiveness of acetaminophen varies based on the cellular peroxide tone. Low peroxide tone allows for effectiveness, while high peroxide tone hinders its action.

A drug that blocks the effects of opioids at the µ receptor, particularly in the central nervous system.

A drug that binds to and activates the µ opioid receptor, producing analgesic and euphoric effects.

A drug that binds to and activates the µ opioid receptor, but with lower affinity than full agonists, reducing adverse effects.

The ability of a drug to produce a desired effect when administered via a specific route.

The state of being dependent on a substance, often leading to withdrawal symptoms upon discontinuation.

A type of therapy that aims to replace one addictive substance with another, less harmful substance.

A type of analgesic that works by inhibiting the production of prostaglandins, which contribute to pain and inflammation.

A medication that interacts with opioid receptors in the body, primarily the µ (mu) receptors, and produces pain relief.

Buprenorphine is a partial agonist of µ receptors, meaning it only partially activates them, and an antagonist of k receptors, meaning it blocks their activation.

Buprenorphine is a very strong µ receptor agonist and a mild k receptor antagonist, resulting in both analgesic and sedative effects.

Buprenorphine is used in addiction reduction programs during the detoxification phase. It helps manage withdrawal symptoms and prevent relapse.

Respiratory depression, a condition where breathing becomes slow and shallow, is a potential side effect of opioids, even at therapeutic doses.

Opioids can cause nausea and vomiting, affecting approximately 40% of individuals due to temporary irritation of the vomiting center.

Opioids suppress the cough reflex, preventing the body from clearing bronchial secretions.

Constipation is a frequent side effect of opioids due to their effects on the gastrointestinal tract.

Paracetamol, also known as acetaminophen, is a common over-the-counter analgesic (pain reliever) and antipyretic (fever reducer) that is often used for mild to moderate pain.

Paracetamol treats pain and fever. It has a slight anti-inflammatory effect, but it's not as potent as NSAIDs.

Paracetamol works by blocking the production of prostaglandins, which are chemicals that cause pain and inflammation. However, it only does this in areas of the body where there is a high concentration of peroxides, such as in inflamed tissue.

Paracetamol can be administered intravenously (i.v.) for short-term treatment of moderate postoperative pain and orally (p.o.) for mild to moderate pain.

Overdose of paracetamol can be lethal, with the lethal dose for adults ranging from 7 to 10 grams.

Paracetamol is primarily metabolized in the liver through two major pathways — glucuronidation and sulfation, which convert the drug into harmless byproducts.

In a second metabolic pathway, paracetamol is broken down by the CYP450 enzymes, producing a toxic intermediate called NAPQI. This is normally detoxified by glutathione, but high doses of paracetamol deplete glutathione and lead to NAPQI buildup.

Symptoms of paracetamol overdose can appear within 4 to 6 days and may include liver failure, encephalopathy, and coma.

A severe liver condition caused by excessive paracetamol intake, leading to damage and dysfunction of the liver.

A common sign of liver damage in paracetamol overdose, usually detected 24-48 hours after ingestion.

A marker of liver dysfunction occurring in paracetamol poisoning, often accompanied by jaundice.

A serious complication of paracetamol overdose indicating severe liver failure; characterized by confusion, drowsiness, and impaired cognitive function.

An antidote given to counteract paracetamol toxicity by restoring glutathione reserves.

The effectiveness of acetylcysteine in treating paracetamol overdose depends on timely administration, ideally within 10 hours after ingestion.

A non-opioid analgesic that inhibits COX in the CNS, reducing the production of PGs and providing an antispasmodic effect.

A potential adverse effect of metamizol, characterized by a significant decrease in white blood cells.