Atherosclerosis begins with endothelial injury caused by hypertension, dyslipidemia, smoking, or hyperglycemia. Damaged endothelium permits infiltration of oxidized LDL into the intima, triggering monocyte recruitment and transformation into foam cells. Smooth muscle cells migrate from the media, forming a fibrous cap over the lipid core. Thin-cap fibroatheromas are vulnerable to rupture, exposing thrombogenic material that activates platelets and the coagulation cascade, forming occlusive thrombus. Inflammatory mediators (IL-6, TNF-alpha, MMP-9) degrade the fibrous cap. The balance between plaque stability (collagen synthesis) and instability (MMP activity) determines clinical outcome. Coronary atherosclerosis manifests as stable angina when stenosis exceeds 70%, while plaque rupture produces acute coronary syndrome regardless of stenosis severity. Peripheral atherosclerosis produces claudication and critical limb ischemia. Cerebrovascular atherosclerosis causes TIA and ischemic stroke. The NP manages modifiable risk factors aggressively: statin therapy reduces LDL and stabilizes plaques via anti-inflammatory effects independent of lipid lowering.