Inflammation and Prostaglandins Overview

A protective response to injury, aiming to remove harmful agents and promote healing.

A constitutive enzyme involved in 'housekeeping' functions.

An enzyme induced by inflammation, often triggered by cytokines.

Molecules that sensitize pain receptors, not the pain initiators.

A pro-inflammatory prostaglandin affecting blood vessels, airways, and pain.

NSAIDs inhibit COX enzymes, reducing prostaglandin production to decrease inflammation and pain.

Specialized sensory neurons that detect and transmit pain signals to the brain.

A prostaglandin inducing uterine contraction and bronchoconstriction.

Ibuprofen is rapidly absorbed after oral ingestion, with a half-life of 1-2 hours.

Ibuprofen is highly bound to plasma proteins, requiring a high dosage (400mg) for noticeable effect.

Ibuprofen metabolites are excreted through the kidneys. Kidney dysfunction is a contraindication.

Ibuprofen is used as an analgesic, antipyretic, anti-inflammatory, to treat acute gouty arthritis, and patent ductus arteriosus, among other uses.

81 mg of aspirin daily inhibits TXA2, preventing platelet aggregation and reducing risk of heart attack, stroke, and colon cancer.

Common adverse effects include gastric upset, fluid retention, hypersensitivity reactions, ocular disturbances, and rare hematologic effects.

Ibuprofen should not be used in peptic ulcer patients, those allergic to aspirin, individuals with kidney impairment, liver disease, or who are pregnant or hemophilic.

Aspirin reduces PGE2 and PGI2, potentially causing vasoconstriction and kidney damage. Patients with low kidney function should avoid.

Ibuprofen can reduce the effectiveness of aspirin's anti-clotting effects.

Aspirin can cause stomach upset, nausea, vomiting, and microscopic bleeding due to inhibiting TXA2's protective effects.

Diclofenac is a more potent anti-inflammatory drug than ibuprofen or Naproxen, and its mechanism is through a more potent cyclooxegenase inhibition.

Aspirin use after viral infection is contraindicated due to risk of Reye Syndrome, a serious but rare condition.

Diclofenac is primarily used in treating inflammatory conditions.

Mild aspirin overdose, marked by nausea, vomiting, headache, dizziness, and tinnitus.

Nonsteroidal anti-inflammatory drugs (NSAIDs) work by inhibiting cyclooxygenase (COX) enzymes, thereby reducing prostaglandin production. This reduces pain and inflammation

Ibuprofen is a reversible COX inhibitor; much like aspirin, but is a more potent anti-inflammatory. It's not affected by the kidney issue of aspirin as long as used for minor pain and fever relief.

Macrophage-released IL-1 stimulates COX-2 in the brain to produce prostaglandins, which trigger the body's thermoregulatory response causing fever

Patients with significantly impaired kidney function (GFR < 30) should not take NSAIDs; safer alternatives like Tylenol should be used instead, especially in patients with existing kidney issues.

TXA2 enhances platelet clumping while PGI2 opposes it. Aspirin inhibits TXA2 without inhibiting PGI2 affecting clotting mechanisms in the blood.

NSAIDs lessen fever by interfering with the production of certain prostaglandins, ultimately reducing the body temperature.

Tissue injury (physical or chemical), and allergic reactions (exposure to antigens in sensitized subjects) cause the release of histamine from mast cells.

Modulates circadian cycles, causes itching, systemic vasodilation, bronchoconstriction, and ileum contraction.

Epinephrine (adrenaline) acts as a physiological antagonist to histamine, often used clinically to counteract histamine's effects, such as bronchoconstriction.

Drugs like cromolyn and nedocromil reduce mast cell degranulation caused by antigens, primarily used to treat asthma and allergic rhinitis.

H2 receptors stimulate gastric secretion, speed up sinus rhythm, cause smooth muscle relaxation, and may inhibit antibody synthesis, T-cell proliferation and cytokine production.

A type of NSAID used to relieve pain and inflammation, but can retain salt and water, potentially increasing blood pressure.

An NSAID preferred for patients with cardiovascular problems because it less likely to cause fluid retention compared to sodium salt.

A short-term NSAID used for acute pain, offering pain management comparable to opioids.

A potent NSAID used for chronic musculoskeletal pain and premature infant PDA closure.

A COX-2 selective NSAID, preferred for osteoarthritis, focusing on inflammation reduction, not pain relief. It is not an analgesic.

Short-term glucocorticoids that reduce inflammation in various conditions. However, they have several side effects.

Local hormones made in tissues; include histamine, prostaglandins, & others, involved in local processes.

A key chemical messenger, relating to allergic and inflammatory responses, gastric secretion, & neurotransmission.

Non-steroidal anti-inflammatory drugs, relieving inflammation and pain.

A prodrug, often preferred for inflammation, converted by the liver. Works with a different mechanism than other NSAIDS.