## Pathophysiology of Varicose Veins **Key Point:** Varicose veins result from valve incompetence and venous wall weakness, NOT from congenital absence of valves. Primary varicose veins arise from degenerative changes in the vein wall and valve leaflets over time, not from developmental absence. ### Correct Statements | Feature | Details | |---------|----------| | **Valve failure mechanism** | Incompetent valves → reflux → increased hydrostatic pressure in distal veins → progressive venous dilation | | **Lipodermatosclerosis** | Chronic venous insufficiency sign; represents skin fibrosis, hyperpigmentation, and induration; precursor to venous ulceration | | **Trendelenburg test** | Positive when saphenofemoral junction (SFJ) is incompetent; limb elevation empties varices, then rapid filling on standing indicates proximal reflux | ### Why Congenital Absence Is Wrong **High-Yield:** Primary varicose veins (90% of cases) develop from: 1. Intrinsic weakness of the vein wall (smooth muscle and elastic fibre deficiency) 2. Degenerative valve changes leading to incompetence 3. Genetic predisposition to venous wall weakness Secondary varicose veins arise from post-thrombotic syndrome, obstruction, or arteriovenous fistula—not from congenital valve absence. **Clinical Pearl:** The distinction is important: if valves were congenitally absent, varicose veins would present in childhood or early adolescence universally; instead, they typically manifest in the 3rd–5th decade. [cite:Sabiston Textbook of Surgery Ch 64]
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