## Pathophysiology of Primary Varicose Veins **Key Point:** Primary varicose veins result from intrinsic weakness of the venous wall (defective collagen and elastin) combined with valve incompetence, NOT from external obstruction or congenital absence. ### Mechanism 1. Defective collagen and elastin in the venous wall → loss of elastic recoil 2. Valve leaflets fail to coapt properly → reflux of blood 3. Increased venous pressure → progressive dilatation and tortuosity 4. Vicious cycle: dilatation → further valve separation → more reflux ### Primary vs. Secondary Varicose Veins | Feature | Primary | Secondary | |---------|---------|----------| | **Cause** | Intrinsic wall weakness + valve incompetence | Post-thrombotic syndrome, obstruction | | **Valve pathology** | Degenerative valve insufficiency | Valve damage from DVT | | **Incidence** | ~90% of all varicose veins | ~10% of all varicose veins | | **Family history** | Often positive (genetic predisposition) | Absent | **High-Yield:** The hallmark of primary varicose veins is valve incompetence demonstrated on Doppler ultrasound (reflux >0.5 seconds in standing position). This distinguishes them from secondary causes. **Clinical Pearl:** Patients with primary varicose veins have normal deep venous system; secondary varicose veins develop when deep veins are damaged or obstructed (e.g., post-DVT).
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