Ans: A (Fatty streaks) Ref: Robbins Pathologic Basis of Disease, 8th edition.Explanation:Fatty streaks are the earliest lesions in atherosclerosis " Ref: RobbinsMorphology of AtherosclerosisFatty StreaksThese are the earliest lesions in atherosclerosis.They are composed of lipid-filled foamy macrophages.Beginning as multiple minute flat yellow spots, they eventually coalesce into elongated streaks 1 cm or more in length.These lesions are not significantly raised and do not cause any flow disturbanceAortas of infants less than 1 year old can exhibit fatty streaks, and such lesions are seen in virtually all children older than 10 years, regardless of geography, race, sex, or environment.The relationship of fatty streaks to atherosclerotic plaques is uncertainThey may evolve into precursors of plaques, not all fatty streaks are destined to become advanced lesions.Atherosclerotic PlaqueThe key processes in atherosclerosis are intimal thickening and lipid accumulationAtheromatous plaques impinge on the lumen of the artery and grossly appear white to yellow: superimposed thrombus over ulcerated plaques is red-brown.Plaques vary from 0.3 to 1.5 cm in diameter but can coalesce to form larger massesAtherosclerotic lesions are patchy, on cross- section, the lesions appear "eccentric"Local flow disturbances (e.g., turbulence at branch points) leads to increased susceptibility to plaque formation.In descending order, the most extensively involved vessels are theLower abdominal aorta (MC)The coronary arteries (Second MC)The popliteal arteriesThe internal carotid arteriesVessels of the circle of WillisVessels of the upper extremities are usually spared, as are the mesenteric and renal arteries, except at their ostia.Atherosclerotic plaques have three principal components:Cells, including smooth muscle cells, macrophages, and T cellsECM, including collagen, elastic fibers, and proteoglycansIntracellular and extracellular lipidSuperficial fibrous cap composed of smooth muscle cells and dense collagen.Beneath and to the side of the cap (the "shoulder") is a more cellular area containing macrophages, T cells, and smooth muscle cells.Deep to the fibrous cap is a necrotic core, containing lipid (primarily cholesterol and cholesterol esters), debris from dead cells, foam cells (lipid-laden macrophages and smooth muscle cells), fibrin, variably organized thrombus, and other plasma proteins and cholesterolThe periphery of the lesions show neovascularization (proliferating small blood vessels;Plaques generally continue to change and progressively enlarge due to cell death and degeneration, synthesis and degradation (remodeling) of ECM, and organization of thrombus.Atheromas often undergo calcificationAtherosclerotic plaques are susceptible to the following clinically important changes* Rupture, ulceration, or erosion of the intimal surface of atheromatous plaques exposes the blood to highly thrombogenic substances and induces thrombosis.* Such thrombosis can partially or completely occlude the lumen and lead to downstream ischemia.* If the patient survives the initial thrombotic occlusion, the clot may become organized and incorporated into the growing plaque.* Hemorrhage into a plaque. Rupture of the overlying fibrous cap, or of the thin-walled vessels in the areas of neovascularization, can cause intra-plaque hemorrhage; a contained hematoma may expand the plaque or induce plaque rupture.* Atheroembolism. Plaque rupture can discharge atherosclerotic debris into the bloodstream, producing microemboli* Alienism formation. Atherosclerosis-induced pressure or ischemic atrophy of the underlying media, with loss of elastic tissue, causes weakness resulting in aneurysmal dilation and potential rupture.