Thrombosis phases

HEMOSTASIS THROMBOSIS HAVE THREE COMMON PHASES... 

In hemostasis, there is initial vasoconstriction of the injured vessel, causing diminished blood flow distal to the injury. Then hemostasis and thrombosis share three phases ... 

Lenalidomide is an immunomodulating agent related to thalidomide that was recently approved for the treatment of patients with multiple myeloma and myelodysplastic syndrome (MDS). Lenalidomide lacks the common side effects of thalidomide, such as constipation and peripheral neuropathy. Interim analyses of two phase III trials show that lenalidomide in combination with dexamethasone produces higher response rates than dexamethasone alone in relapsed and refractory myeloma. Adverse effects of lenalidomide include diarrhea, nausea, muscle cramps, hematologic side effects and deep vein thrombosis.42... 

The ideal anticoagulant drug would prevent pathologic thrombosis and limit reperfusion injury, yet allow a normal response to vascular injury and limit bleeding. Theoretically this could be accomplished by preservation of the TF-VIIa initiation phase of the clotting mechanism with attenuation of the secondary intrinsic pathway propagation phase of clot development. At this... 

A major focus of drug development has been to develop orally active anticoagulants that do not require monitoring. Rivaroxiban is the first oral factor Xa inhibitor to reach phase III clinical trials. The safety and efficacy of rivaroxiban appears to be at least equivalent, and possibly superior, to LMW heparins for prevention of deep vein thrombosis no routine monitoring is required. This drug is also in clinical trials for treatment of deep vein thrombosis and prevention of stroke in atrial fibrillation. 

Elevated TAFI levels have been found in men with symptomatic coronary artery disease (142). TAFI is also reported to be a risk factor for deep venous thrombosis, A recent report on the high levels of TAFI in the acute phase of ischemic stroke revealed not only elevated levels but also an incremental increase in TAFI with the degree of neurologic deterioration (143). Therefore, the observation by Boffa et al. on the acute phase nature of this protein requires further validation, In addition, Juhan-Vague et al, stated that there is a correlation between TAFI levels and cardiovascular risk factors (144). Animal models may be needed to truly validate studies on TAFI upregulation and its relation to thrombosis. 

The compounds potently inhibit factor Xa in vitro with reversible binding kinetics and are able to inhibit not only free but also prothrombinase-bound factor Xa (Ki 41 nM, 0.1 I nM, and 0,5 nM, respectively) (58-60), In contrast, no direct effect on platelet aggregation has been described (60-62), Antithrombotic activity in arterial and venous thrombosis models has been demonstrated and it has a reduced effect on hemorrhage in comparison to standard therapy (58,60,63). Factor Xa inhibitors are able to reduce the endogenous thrombin potential in platelet-poor as well as in platelet-rich plasma (64,65). Thus, thrombin generation seems to be a suitable biomarker for clinical evaluation and has been evaluated in phase I studies (66,67). 

Benedict et al. (1986) introduced a procedure in which anodal current is discontinued when mean distal coronary flow velocity increased by approximately 50%, reflecting disruption of normal flow by the growing thrombus. Occlusive thrombosis occurred within 1 h after stopping the electrical current. It was observed that the final phase of thrombosis occurred independently of electrical injury. 

Magnetic resonance imaging has greater sensitivity than CT for the changes of cerebral venous thrombosis (Bousser and Ross Russell 1997 Ferro et at 2007). In the acute phase, at less than three to five days, the thrombus is isointense on both Ti- and T2-weighted sequences. Subsequently, the thrombus becomes hyperintense (Fig. 29.3). After two to three weeks, findings depend on whether or not the sinus remains occluded or whether it is partly or completely recanalized. 

Peripheral arterial occlusion. Heparin may prevent extension of a thrombus and hasten its recanalisation it is commonly used in the acute phase following thrombosis or embolism. There is no case for treating ischaemic peripheral vascular disease with an oral anticoagulant (for prevention, see Antiplatelet drugs). 

Thromboses in the vessels of the portal system constitute the most common cause of prehepatic portal hypertension. Even in the postpartal phase, portal vein thrombosis may occur due to the obliteration of the umbilical vein spreading to the portal vein or due to an infection of the umbilical vein with subsequent pylephlebitis. In the adult, this clinical picture is most commonly observed in liver diseases that cause the portal blood flow to slow down (or even reverse). All diseases which are accompanied by hypercoagulopathies also have a strong tendency to cause portal vein thrombosis. (106, 110, 112, 119, 121) Patients with liver cell carcinoma due to cirrhosis quite often develop thrombosis. Septic processes (such as appendicitis, diverticulitis, colitis) are a further common cause, particularly in immuno-... 

Ginsenoside Rgi had no effect on arachidonate metabolism, but it did reduce the elevation of cytosolic free calcium concentration [Ca2+]i shown in the second phase (Ca2+ influx) induced by adrenaline and thrombin "Fig. (37)". The results suggest that ginsenoside Rgl in red ginseng roots may be effective as a drug for the treatment of arteriosclerosis and thrombosis. 

Necrotic phase This phase occurs 1-4 days after injury. Cells die from coagulation of intracellular protein. Vascular thrombosis and bacterial invasion may worsen the underlying injury. The esophagus is especially vulnerable to perforation during this phase. 

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