All of the following regarding venous anatomy is true EXCEPT:
Veins are thin-walled, highly distensible, and collapsible. Their structure specifically supports the primary functions of veins to transport blood toward the heart and serve as a reservoir to prevent intravascular volume overload. The venous intima is composed of a nonthrombogenic endothelium with an underlying basement membrane and an elastic lamina. The endothelium produces endotheliumderived relaxing factors such as nitric oxide and prostacyclin, which help maintain a nonthrombogenic surface through inhibition of platelet aggregation and promotion of platelet disaggregation. Circumferential rings of elastic tissue and smooth muscle located in the media of the vein allow for changes in vein caliber with minimal changes in venous pressure. The adventitia is most prominent in large veins and consists of collagen, elastic fibers, and fibroblasts. When a vein is maximally distended, its diameter may be several times greater than that in the supine position. In the axial veins, unidirectional blood flow is achieved with multiple venous valves. The inferior vena cava (IVC), common iliac veins, portal venous system, and cranial sinuses are valveless. In the axial veins, valves are more numerous distally in the extremities than proximally. Each valve consists of two thin cusps of a fine connective tissue skeleton covered by endothelium. Venous valves close in response to cephaladto-caudal blood flow at a velocity of at least 30 cm/s2.
Chronic venous insufficiency ( CVI) is characterized by all of the following EXCEPT:
Chronic venous insufficiency ( CVI) may lead to characteristic changes in the skin and subcutaneous tissues in the affected limb. CVI results from incompetence of venous valves, venous obstruction, or both. Most CVI involves venous reflux, and severe CVI often reflects a combination of reflux and venous obstruction. It is important to remember that although CVI originates with abnormalities of the veins, the target organ of CVI is the skin, and the underlying physiologic and biochemical mechanisms leading to the cutaneous abnormalities associated with CVI are poorly understood. A typical leg affected by CVI will be edematous, with edema increasing over the course of the day. The leg may also be indurated and pigmented with eczema and dermatitis. These changes are associated with excessive proteinaceous capillary exudate and deposition of a pericapillary fibrin cuff that may limit nutritional exchange. In addition, an increase in white blood cell (WBC) trapping within the skin microcirculation in CVI patients may lead to microvascular congestion and thrombosis. Subsequently, WBCs may migrate into the interstitium and release necrotizing lysosomal enzymes, potentially leading to tissue destruction and eventual ulceration. Fibrosis can eventually develop from impaired nutrition, chronic inflammation, and fat necrosis (lipodermatosclerosis). Hemosiderin deposition due to the extravasation of red cells and subsequent lysis in the skin contributes to the characteristic pigmentation of chronic venous disease (Fig. below). Ulceration can develop with longstanding venous hypertension and is associated with alterations in microcirculatory and cutaneous lymphatic anatomy and function. The most common location of venous ulceration is approximately 3 cm proximal to the medial malleolus (Fig. below).
Characteristic hyperpigmentation of chronic venous insufficiency.
Venous ulceration located proximal to the medial malleolus.
Venous thromboembolism (VTE) is associated with all of the following EXCEPT:
The incidence of venous thromboembolism (VTE) is approximately 100 per 100,000 people per year in the general population, with 20% of the diagnoses made within 3 months of a surgical procedure. Of the symptomatic patients, one-third will present with pulmonary embolism (PE) and two-thirds with deep vein thrombosis (DVT). The estimated number of cases of VTE may well be over 600,000 per year in the United States, making it a major U.S. health problem. Furthermore, death occurs in 6% of DVT and 12% of PE cases within 1 month of diagnosis. Not only does VTE pose a veritable threat to life, but it also places patients at higher risk for recurrence and post-VTE sequelae such as pulmonary hypertension and postthrombotic syndrome, with 4% and up to 30% incidence, respectively.
Virchow triad is characterized by:
Three conditions, first described by Rudolf Virchow in 1862, contribute to VTE formation: stasis ofblood flow, endothelial damage, and hypercoagulability. Of these risk factors, relative hypercoagulability appears most important in most cases of spontaneous VTE, or so-called idiopathic VTE, whereas stasis and endothelial damage likely play a greater role in secondary VTE, or so-called provoked VTE, occurring in association with transient risk factors such as immobilization, surgical procedures, and trauma.
Risk factors for inherited VTE include all of the following EXCEPT:
Von Willebrand Disease is the most common genetic bleeding disorder and is characterized by a propensity to bleed. All other disorders listed are associated with increased risk of VTE.
Risk factors for venous thromboembolism:
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