Venous focal

The vascular tree is divided into two main, well-demarcated areas composed of the arterial and the venous trees. They both define different microenvironments that create the conditions for the development of focal episodes determining the occurrence of obstructive phenomena that are at the base of CVD. Arterial episodes (CHD and stroke) occur at sites of inflamed arteries, while VTED or venous stroke episodes develop as a result of thrombus formation at discrete locations in the venous tree. 

Hypercoagulable states, in turn, have been traditionally associated with venous thrombosis. Consequently, attention has been paid to alterations of the hemostatic balance. Although this is a systemic variable, focality is favored due to the contribution of decreased blood flow, as confirmed by the preferential development of venous thrombi at the level of valves, an area of stasis where low-velocity flow is moderately turbulent. 

In conclusion, hemostasia intervenes in distinct critical steps of both the arterial and venous forms of CVD. The particulars, however, differ in each case, as confirmed by the different array of risk factors for CHD and VTED. The participation of the vascular wall is pivotal in explaining the focality of these processes. Within the vascular wall, the role of the endothelium is critical given its involvement in the origin of atherosclerosis and its influence on the development of VTED (for review see Cano and Van Baal 2001 Cano 2003). 

Neurological involvement in Behcet s disease may be subclassified into two major forms a vascular-inflammatory process with focal or multifocal parenchymal involvement and a cerebral venous sinus thrombosis with intracranial hypertension. The vasculitis and meningitis may affect cerebral arteries, particularly in the posterior circulation, to cause ischemic stroke and possibly intracranial hemorrhage (Farah et al. 1998 Krespi et al 2001 Siva et al. 2004 Borhani Haghighi et al. 2005). 

Cerebrospinal fluid is often abnormal in cerebral venous thrombosis the pressure is usually raised and there may be elevated protein and pleocytosis, especially in patients with focal signs. Lumbar puncture may be indicated in patients with isolated intracranial hypertension in order to lower cerebrospinal fluid pressure when vision is threatened and to exclude meningeal infection. 

Focal nodular hyperplasia On MRI scans (as with CT), FNH shows the characteristic central venous star. Otherwise, the signal intensity of FNH is homogeneously isointense (Ti) or slightly hyperintense (T2). Immediately following the i.v. administration of CM (Gd-DTPA), a distinct but rapidly fading enhancement is observed. (65, 95, 100, 102, 110, 118)... 

In the Budd-Chiari syndrome, the central area of the liver shows a normal or even increased concentration of radioactivity, whereas the peripheral regions of both lobes of liver exhibit reduced or even no uptake ( hot spots and multiple focal storage defects). Only the caudate lobe shows increased activity due to its separate venous flow, it is not functionally affected by hepatic vein thrombosis. (26)... 

Biopsy specimens of PAH include constrictive lesions and complex lesions. Constrictive lesions comprise medial hypertrophy and intimal thickening. Medial hypertrophy is defined as the increase in both number and cross-sectional area of the SM cells lining the walls of the pre- and intra-acinar pulmonary arteries intimal thickening implies an increased number of fibroblasts in the thin layer between a SM cell and lamina propria of the blood vessel. These changes can be seen in both IPAH and pulmonary venous hypertension. In contrast, complex lesions are considered pathognomonic for PAH. The complex or plexiform lesion consists of focal proliferation of endothelial channels consisting of fibroblasts, SM cells, and connective tissue matrix. These lesions disrupt vascular vessel wall and serve as a nidus for in situ thrombosis. 

Liver biopsy specimens from eight cases, and autopsy material from one human case and two dogs were studied. Characteristic features were centrizonal scarring, hepatic venous occlusion, ductular proliferation and cholestasis, focal S mcytial giant-cell transformation of hepatocytes, and pericellular fibrosis. 

Cerebral venous sinus thrombosis (CVT) is a rare condition that affects 3 per 1,000,000, approximately 0.5% of all adult stroke cases (Table 7.9) [138, 139]. The most common presenting signs and symptoms are headache, seizures, vomiting, and papilledema. Visual changes, altered consciousness, cranial nerve palsies, nystagmus, and focal neurologic deficits are also... 

The appropriate examination technique is critical for sensitive detection and specific characterization of focal liver lesions. A biphasic examination of the liver with a late-arterial and a portal venous phase can be regarded as standard today. For specific indications, like the follow-up of hepatocellular carcinoma (HCC) after transarterial chemoembolization (TACE) or for the depiction of the arterial vessels prior to angiography, an early arterial phase scan, which can be post-processed into CT angiography, is helpful (Fig. 3.2). The value of delayed scans (e.g. 5 min after contrast agent injection) is controversial in the literature mainly centers with a focus on imaging in liver cirrhosis consider the use of late phase images as necessary, whereas other authors see no added value for it [21,45]. 

If one plans to perform two scans, the liver can be scanned from bottom to top. In this way, there is better venous enhancement at the end of the scan, which reduces the risk of mistaking unfilled veins of the venous confluence above the liver for focal liver lesions. Another advantage of this direction is that one can continue to scan where required. Subsequently, the pelvis is examined dming a second breath-hold. 

Details of follicular formation and ovulation remain unsettled. There is some indication that the liquor is formed by filtration of plasma rather than as a result of venous or lymphatic obstruction. Increased hydrostatic pressure in the follicle is unlikely to cause its rupture. Rupture seems to result from focal alteration of the site of the stigma. Electron microscopic examination of the stimaga reveals collagen digestion and cell separation. 

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