Diseases of the veins

Varicose veins: Varicose veins are abnormally dilated, tortuous veins. They are most commonly seen in the legs, followed by the lower esophagus, hemorrhoids in the anal region, and the spermatic cord as varicoceles. In the lower leg, the long saphenous vein is commonly affected. Varicose veins are more common in females.

They’re exacerbated by venous stasis due to increased venous pressure, especially when venous drainage is obstructed. Predisposing factors include occupations that require prolonged standing (e.g., surgeons, nurses), pregnancy, pelvic tumors, obesity, chronic constipation, and menopausal hormonal changes.

A key mechanism is venous valve incompetence in perforator branches. This allows backflow of venous blood from the deep venous system to the superficial venous system in the legs, leading to superficial varicosities. DVT can also cause varicosities: when deep veins are blocked, venous blood is diverted retrograde into superficial veins.

Stasis or venous ulcers and stasis dermatitis: Venous ulcers are the most common type of ulcers. They’re seen in DVT, venous insufficiency, and thrombophlebitis. The underlying cause is venous hypertension, which leads to venous stasis and inflammation. Endothelial damage and platelet aggregation interfere with local circulation, contributing to ulcer formation. These ulcers may persist for weeks to years. Complications include osteomyelitis, cellulitis, malignancy, etc.

Stasis dermatitis refers to skin changes seen in chronic venous insufficiency. It typically appears bilaterally around the medial malleolus as erythematous plaques and eczema-like patches, often with hyperpigmentation. It can progress to ulcer formation, bacterial superinfections, and lipodermatosclerosis (panniculitis, or inflammation of subcutaneous fat in the lower legs). Lipodermatosclerosis can cause tapering of the legs, producing an “inverted champagne bottle” sign.

The underlying mechanism is venous hypertension, which increases hydrostatic pressure in capillaries. This increases vascular permeability and leads to transudation of fibrinogen into tissues, triggering local inflammation. Formation of fibrin cuffs is specific for stasis dermatitis.

Thrombophlebitis and phlebothrombosis: The key difference between thrombophlebitis and phlebothrombosis is the presence of inflammation in thrombophlebitis. Virchow triad - venous stasis, hypercoagulability, and endothelial damage - predisposes to venous thrombosis. The most common sites are the deep veins of the legs, followed by the periprostatic plexus, pelvic veins, and veins near infected foci (e.g., appendicitis).

Thrombophlebitis presents with pain and tenderness along the course of a vein. Inflamed veins may be palpable as tender, cord-like structures. Example: Mondor’s disease is thrombophlebitis of superficial veins of the breast and anterior chest wall.

Migratory thrombophlebitis (Trousseau’s syndrome) is seen in cancers of the pancreas, prostate, lungs, gastrointestinal tract, etc. Multiple venous thrombi occur in different areas and may appear to “move” from one site to another.

VIII) Vascular neoplasms: Myxoma is the most common primary tumor of the heart. The most common location is the left atrium. Microscopically, it shows sparse, stellate or spindle-shaped cells in an abundant myxoid, mucinous stroma.

Metastases to the heart - from primary tumors in the lung, breast, leukemias and lymphomas, and malignant melanomas - are the most common cardiac tumors.