Exam IV: Pathology of Vascular Interventions Flashcards
Varicose Veins
Abnormally dilated, tortuous veins (serpentine)
Causes prolonged, increased intraluminal pressure and loss of vessel wall support
Involvement: superficial veins of the upper and lower leg
Varicose Veins: Causes and Complications
Familial tendency: development of varicosities due to defective development of vein walls
Most disabling complications:
- Persistent edema in the extremity
- Ischemic skin changes: stasis dermatitis and cutaneous ulcerations due to poor wound healing and superimposed infections; can develop chronic varicose ulcers
Esophageal Varices
Liver cirrhosis causes portal vein hypertension, which opens porto-systemic shunts to increase blood flow into veins at esophagealgastic junction
Development of:
- Esophageal varices
- Rectum (hemorrhoids)
- Periumbilical veins of abdominal wall (caput medusa)
Most important: rupture causes massive (fatal) upper GI hemorrhage
Thrombophlebitis/Phlebothrombosis
Venous thrombosis + inflammation
Venous thrombosis: potentiated by cardiac failure, neoplasia, pregnancy, obesity, post-op state, prolonged bed rest/immobilization
Deep leg veins account for > 90% of thrombophlebitis cases
Riding in a plane for a long time without moving
Surgery on knee or hip, or some type of immobilization then DVT to PE
Thrombophlebitis/Phlebothrombosis: Other Sites
Other sites:
Periprostatic venous plexus (males)
Pelvic venous plexus (females)
Large veins in the skull and the dural sinuses (infection or inflammation)
Portal vein thrombosis
Peritoneal infections, appendicitis, salpingitis, and pelvic abscesses
Thrombophlebitis/Phlebothrombosis: Systemic Hypercoagulability
Carcinoma: adenocarcinomas cause paraneoplastic syndrome, which is a pro-coagulant state caused by factors by the tumor cells
Migratory thrombophlebitis: AKA thrombophlebitis migrans
Trousseau sign of malignancy
Venous thrombi occur in one site and reappear elsewhere
Pulmonary Embolism (PE)
Serious complication of DVT
Fragmentation/detachment of whole venous thrombus
First manifestation of thrombophlebitis
Lymphangitis
Bacterial infections spread into and through lymphatics:
Acute inflammation in lymphatic channels/nodes
Most common agent: Group A β-hemolytic streptococci
Affected lymphatics:
Dilated and filled with inflammatory infiltrate composed of neutrophils (acute) and histiocytes (starting to become chronic)
Extends through the vessel wall
Perilymphatic tissues
Cellulitis or focal abscesses (severe cases)
Clinical Features of Lymphangitis
Painful subcutaneous red streaks extend along the course of lymphatics
Painful enlargement of regional lymph nodes
If lymph nodes fail to block bacteria they drain into venous circulation causing bacteremia or septicemia
Primary Lymphedema
Isolated congenital defect (simple congenital lymphedema)
Familial Milroy disease: heredofamilial congenital lymphedema that causes lymphatic agenesis or hypoplasia
The patient will have no lymph nodes or no nodes in that appendage
Secondary (Obstructive) Lymphedema
Occlusion of lymphatic vessels causing abnormal accumulation of interstitial fluid
Most common causes:
- Malignant tumors obstructing lymphatic channels or regional lymph nodes
- Surgical procedures that remove regional groups of lymph nodes- axillary lymph nodes in radical mastectomy
- Post-irradiation fibrosis
- Filariasis- causes elephantitis; larvae of microfilariae that hatch and block fluid
- Post-inflammatory thrombosis and scarring
Persistence of Lymphedema
Increase of subcutaneous interstitial fibrous tissue
Consequent enlargement of affected part
Induration: peau d’orange (orange peel) appearance and skin ulcers
Lymphedema in Cavities
Milky collections of lymph in various spaces
Rupture of dilated lymphatics due to obstruction of lymphatics by infiltrating tumor
Categories:
Chylous ascites (peritoneum)
Chylothorax (pleural cavity)
Chylopericardium (pericardium)
Benign Hemangiomas
Locally aggressive lesions with infrequent metastases
Rarely highly malignant angiosarcomas
Primary tumors of large vessels:
Aorta, pulmonary artery, and vena cava
Extremely rare and mostly connective tissue sarcomas
Extremely common tumors
Increased numbers of normal or abnormal vessels filled with blood
Majority are superficial lesions in head or neck
Internal lesions: 1/3rd in the liver
Many types/variations: capillary, cavernous, and pyogenic granuloma
Vascular Neoplasms
Endothelium-derived: hemangioma, lymphangioma, angiosarcoma
Arise from cells that support and/or surround blood vessels such as endothelial and glomus cells
Glomus tumor, hemangiopericytoma
Capillary Hemangioma
Most common variant
Composed of a proliferation of benign capillaries
Locations:
Skin and subcutaneous tissues
Mucous membranes of the oral cavities and lips
Liver, spleen, and kidneys
Capillary Hemangioma Characteristics
Bright red to blue
Millimeters to several centimeters in diameter
Flat or elevated
Unencapsulated aggregates of closely packed, thin-walled capillaries- blood-filled and lined by flattened endothelium
Scant connective tissue stroma separates vessels
Lumens may be partially or completely thrombosed
Microscopically: everything looks well maintained, just see a lot of capillaries
Capillary Hemangioma: Strawberry Type
AKA Juvenile hemangioma of the skin of newborns
Extremely common
May be multiple
Grows rapidly in the first few months
Fades at 1 to 3 years of age
Completely regresses by age 7 (75% to 90% of cases)
Cavernous Hemangioma
Large, dilated vascular channels
Less well circumscribed
Involve deep structures
Brain hemangiomas–most problematic because pressure symptoms or rupture
Component of von Hippel-Lindau disease: cerebellum, brain stem, or retina