Inflammation is a complex, coordinated biological response to tissue injury, infection, or foreign substances that involves the vascular system, immune cells, and molecular mediators. The NP must understand the molecular cascade to interpret inflammatory biomarkers, select appropriate anti-inflammatory therapies, and differentiate physiological from pathological inflammation. Acute Inflammation: The acute inflammatory response is initiated within seconds to minutes of tissue injury and involves three primary phases: vascular changes, cellular recruitment, and resolution. Tissue-resident macrophages and mast cells serve as sentinels, detecting damage-associated molecular patterns (DAMPs) from injured cells (ATP, HMGB1, uric acid crystals) and pathogen-associated molecular patterns (PAMPs) through pattern recognition receptors (TLRs, NOD-like receptors). Mast cell degranulation releases preformed mediators — histamine, serotonin, and TNF-α — causing immediate arteriolar vasodilation and increased vascular permeability. Histamine acts on H1 receptors on endothelial cells, causing contraction of endothelial cells and widening of intercellular gaps, allowing protein-rich exudate to leak into the interstitium. This produces the cardinal signs of inflammation: rubor (redness from vasodilation), calor (heat from increased blood flow), tumor (swelling from edema), dolor (pain from bradykinin and prostaglandins sensitizing nociceptors), and...