Secondary Raynaud phenomenon refers to vascular insufficiency due to arterial disease caused by other entities including systemic lupus erythematosus, scleroderma, Buerger disease, or even atherosclerosis. Indeed, since Raynaud phenomenon may be the first manifestation of such conditions, every patient with Raynaud phenomenon should be evaluated for these secondary causes.
Vasospasm of cardiac arterial or arteriolar beds has been called cardiac Raynaud and in a subset of cases leads to Prinzmetal angina (angina due to vasospasm). If such spasm is of sufficient duration (20 to 30 minutes), myocardial infarction can result. Elevated levels of catechols also increase heart rate and myocardial contractility, exacerbating ischemia caused by the vasospasm. The outcome can be sudden cardiac death (caused by a fatal arrhythmia) or an ischemic dilated cardiomyopathy—so-called “Takotsubo cardiomyopathy” (also called “broken heart syndrome,” because of the association with emotional duress). Histologic findings in acute cases may include microscopic areas of necrosis characterized by myocyte hypercontraction (contraction band necrosis) (Chapter 11); in subacute and chronic cases, microscopic foci of granulation tissue and/or scar may be present.
Varicose veins and phlebothrombosis/thrombophlebitis account for at least 90% of cases of clinically relevant venous disease.
Varicose veins are abnormally dilated tortuous veins produced by chronically increased intraluminal pressures and weakened vessel wall support. The superficial veins of the upper and lower leg typically are involved. Up to one fifth of men and one third of women develop lower-extremity varicose veins. Obesity increases the risk, and the higher incidence in women probably reflects the prolonged elevation in venous pressure caused by compression of the inferior vena cava by the gravid uterus during pregnancy. There is also a familial tendency toward premature varicosities.
Varicose dilation renders the venous valves incompetent and leads to lower-extremity stasis, congestion, edema, pain, and thrombosis. The most disabling sequelae include persistent edema in the extremity and secondary ischemic skin changes, including stasis dermatitis and ulcerations. The latter can become chronic varicose ulcers as a consequence of poor wound healing and superimposed infections. Of note, embolism from these superficial veins is very rare, in contrast with the relatively frequent emboli that arise from thrombosed deep veins (Chapter 4).
Venous dilations in two other sites merit special attention: • Esophageal varices. Liver cirrhosis (and less frequently, portal vein obstruction or hepatic vein thrombosis) causes portal venous hypertension (Chapter 16). This, in turn, leads to the opening of porto-systemic shunts and increased blood flow into veins at the (1) gastroesophageal junction (forming esophageal varices); (2) rectum (forming hemorrhoids); and (3) periumbilical veins of the abdominal wall (forming a caput medusae). Esophageal varices are most important since they are prone to ruptures that can lead to massive (even fatal) upper gastrointestinal hemorrhage.
http://ebooksmedicine.net • Hemorrhoids are varicose dilations of the venous plexus at the anorectal junction that result from prolonged pelvic vascular congestion associated with pregnancy or straining to defecate. Hemorrhoids are a source of bleeding and are prone to thrombosis and painful ulceration.
Thrombosis of deep leg veins accounts for more than 90% of cases of thrombophlebitis and phlebothrombosis.