Thrombosis and

Deficiency of Factor VII is relatively rare and inherited as an autosomal recessive disorder. Deficiency of Factor VII has been reported to be associated with bond abnormal bleeding and thrombotic tendencies. Deep vein thrombosis and pulmonary emboli have been reported in affected individuals. There is a very high frequency of Factor VII deficiency in people with the Dubin-Johnson syndrome, which is a congenital disorder of Hver function. 

Indications for treatment with streptokinase include acute occlusion of arteries, deep vein thrombosis, and pulmonary embolism. Streptokinase therapy in coronary thrombosis, which is the usual cause of myocardial infarction (54,71,72), has proved to be valuable. In this frequently fatal condition, the enzyme is adrninistered intravenously at a dose of 1.5 million units over 60 min, or given by intracoronary infusion at a 20,000- to 50,000-unit bolus dose followed by 2000 to 4000 units/min for 60 min therapy must be instituted as soon as practicable after the diagnosis of heart attack is made. For deep vein thrombosis, pulmonary embolism, or arterial occlusion, streptokinase is infused at a loading dose of 250,000 units given over 30 min, followed by a maintenance dose of 100,000 units over a 60-min period. 

The IV solutions of plasma expanders include hetastarch (Hespan), low-molecular-weight dextran (Dextran 40), and high-molecular-weight dextran (Dextran 70, Dextran 75). Plasma expanders are used to expand plasma volume when shock is caused by bums, hemorrhage surgery, and otiier trauma and for prophylaxis of venous thrombosis and diromboembolism. When used in die treatment of shock, plasma expanders are not a substitute for whole blood or plasma, but tiiey are of value as emergency measures until die latter substances can be used. 

Arnold R, Kim R, Zhou Y, Tang B. Budgetary impact of heparin-induced thrombocytopenia with thrombosis and treatment with the direct thrombin inhibitor Argatroban (P401E). ASHP 39th Midyear Clinical Meeting. Orlando, FL, 2004. 

Supplements of 400 Ig/d of folate begun before conception result in a significant reduction in the incidence of neural mbe defects as found in spina bifida. Elevated blood homocysteine is an associated risk factor for atherosclerosis, thrombosis, and hypertension. The condition is due to impaired abihty to form methyl-tetrahydrofolate by methylene-tetrahydrofolate reductase, causing functional folate deficiency and resulting in failure to remethylate homocysteine to methionine. People with the causative abnormal variant of methylene-tetrahydrofolate reductase do not develop hyperhomocysteinemia if they have a relatively high intake of folate, but it is not yet known whether this affects the incidence of cardiovascular disease. 

Heparin and warfarin are widely used in the treatment of thrombotic and thromboembolic conditions, such as deep vein thrombosis and pulmonary embolus. Heparin is administered first, because of its prompt onset of action, whereas warfarin takes several days to reach full effect. Their effects are closely monitored by use of appropriate tests of coagulation (see below) because of the risk of producing hemorrhage. 

TableS1-4. Molecules synthesized by endothelial cells that play a role in the regulation of thrombosis and fibrinolysis. ...

Adapted from Wu KK Endothelial cells in hemostasis, thrombosis and inflammation. Hosp Pract (Off Ed) 1992 Apr 27 145. 

Streptokinase is administered by intravenous or intra-arterial infusion in the treatment of thrombo-embolic disorders, e g. pulmonary embolism, deep-vein thrombosis and arterial occlusiorrs. It is also used in acute myocardial irtfarclioa... 

Acute anticoagulation is widely used in the acute setting of arterial dissection. Once again, the rationale is to prevent propagation of local thrombosis and formation of new thrombus at the site of the injured arterial wall, which is beheved to reduce the likelihood of early stroke recurrence. This practice, while rational, is based on anecdotal evidence and case series, as randomized controlled trials have... 

Kamphuisen PW, Agnelli G. What is the optimal pharmacological prophylaxis for the prevention of deep-vein thrombosis and pulmonary embolism in patients with acute ischemic stroke Thromb Res 2007 119(3) 265-274. 

RAJAVASHISTH T B, YAMADA H and MiSHRA N K (1995) Transcriptional activation of macrophage stimulating factor gene by minimally modified LDL Arteriosclerosis, Thrombosis and Vascular Biology 15, 1591-8. 

FRUEBis J, GONZALEZ v, siLVESTRE M and PALiNSKi w (1997) Effect of probucol treatment on gene expression of VCAM-1, MCP-1, and M-CSF in the aortic wall of LDL receptor-deficient rabbits during early sihsro genss.is, Arteriosclerosis, Thrombosis and Vascular Biology 17, 1289-302. 

BHAKDi s (1998) Atherogenic properties of enzymatically degraded LDL selective induction of MCP-1 and cytotoxic effects on human macrophages Arteriosclerosis, Thrombosis and Vascular Biology 18, 1376-85. 

Selective inhibition of tumor necrosis factor-induced vascular cell adhesion molecule-1 gene expression by a novel flavonoid. Lack of effect on trascriptional factor NF-kB Arteriosclerosis, Thrombosis and Vascular Biology 16, 1501-8. 

HAYEK T, FURHMAN B, VAYA J, ROSENBLAT M, BELINRY P, COLEMAN R, ELIS A, AVIRAM M (1997) Reduced progression of atherosclerosis in apolipoprotein E-deficient mice following consiunption of red wine, or its polyphenols quercetin or catechin, is associated with reduced susceptibility of LDL to oxidation aggregation, Arteriosclerosis, Thrombosis and Vascular Biology, 17, 2744-52. 

PRINCEN H M, VAN DUYVENVOORDE W, BUYTENHEK R, BLONK C, TIJBURG L B, LANGIUS J A, MEINDERS A E, PUL H (1998) No effect of consiunption of green and black tea on plasma lipid antioxidant level and on LDL oxidation in smokers, Arteriosclerosis, Thrombosis and Vascular Biology, 18, 833-41. 

Management of Deep-Vein Thrombosis and Pulmonary Embolism... 

Identify risk factors and signs and symptoms of deep vein thrombosis and pulmonary embolism. 

Complications associated with HD include hypotension, myalgia, thrombosis, and infection. 

Fungal vascular invasion, thrombosis, and infarction seen in computer tomographic scan of lungs... 

Lenalidomide was approved recently for the indication of myelodysplastic syndrome where the 5q deletion is present. Since lenalidomide is an analog of thalidomide, all the same precautions must be taken to prevent phocomelia. The time to maximum lenalidomide concentrations occurs 0.5 to 4 hours after the dose. The terminal half-life ranges from 3 to 9 hours. Approximately 65% of lenalidomide is eliminated unchanged in the urine, with clearance exceeding the glomerular filtration rate. To date, no pharmacokinetic studies have been done in patients with renal dysfunction. Lenalidomide is used in the treatment of myelodysplastic syndrome and multiple myeloma. Other side effects are neutropenia, thrombocytopenia, deep vein thrombosis, and pulmonary embolus. 

Mechanical complications of PN are related to catheter placement and the system and equipment used to administer PN. A central venous catheter must be placed by a trained professional, and risks associated with placement include pneumothorax, arterial puncture, bleeding, hematoma formation, venous thrombosis, and air embolism.1,20 Over time, the catheter may require replacement. Problems with the equipment include malfunctions of the infusion pump, intravenous tubing sets, and filters. 

Fig. 11.1. Atherogenesis is a persistent inflammatory response that occurs in response to conditions that cause endothelial damage (e.g., hypercholesterolemia and oxLDL). After endothelial cells are activated, they elaborate cytokines, chemokines, and other mediators that recruit mononuclear cells (monocytes and T lymphocytes) to extravasate into the vessel wall where they are activated and release additional proinflammatory factors. Macrophages are able to take up oxLDL via scavenger receptors causing them to differentiate into foam cells and form a fatty streak that progresses to an atheroma with a necrotic lipid core and a fibrous cap. Chemokines can lead to weakening of the fibrous cap and eventual plaque rupture leading to thrombosis and occlusion of the involved vessel.

Without going into the molecular defects in other coagulation factors, suffice it to say that our current understanding of mechanisms leading to the clinical expression of thrombosis and bleeding has been enhanced by the knowledge of such mutations. 

Eriksson B. I., Kalebo P Anthmyr B. A., et al. Prevention of deep-vein thrombosis and pulmonary embolism after total hip replacement. Comparison of low molecular weight heparin and unfractionated heparin. J Bone Joint Surg [Am] 1991 73A, 484-93. 

Fareed J., Bick R. L., Hoppensteadt D. A., Bermes E. W. Molecular markers of hemostatic activation Applications in the diagnosis of thrombosis and vascular and thrombotic disorders. Clin Appl Thromb Haemost 1995 1, 87-102. 

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