Thrombosis development

Mild thrombocytopenia - Mild thrombocytopenia may remain stable or reverse even if heparin is continued. However, closely monitor thrombocytopenia of any degree. If a count falls below 100,000/mm or if recurrent thrombosis develops, discontinue heparin. If continued heparin therapy is essential, administration of heparin from a different organ source can be reinstituted with caution. 

Cerebral vein thrombosis developed after the administration of 10 mg of phytomenadione in two patients with chronic intestinal inflammation assumed to be part of an autoimmune disease (2). 

In a study in 100 patients with newly diagnosed multiple myeloma given induction chemotherapy (dexamethasone, vincristine, doxorubicin, cyclophosphamide, etoposide and cisplatin) with or without thalidomide, deep vein thrombosis developed in 14 of the 50 patients (28%) given thalidomide compared with 2 of 50 patients (4%) not given thalidomide. Deep vein thrombosis has been reported to occur in 10% of patients treated for multiple myeloma but is reported to occur in about 2% in patients with multiple myeloma treated with thalidomide alone. ... 

Thrombosis is the development of a thrombus , consisting of platelets, fibrin, red and white blood cells in the arterial or venous circulation. Platelet-rich white thrombi are found in the arterial system and can be prevented by antiplatelet drugs. 

Ms. Jackson, age 56years, is hospitalized with a venous thrombosis. The primary health care provider orders SC heparin. In developing a care plan for Ms. Jiekson, discuss the nursing interventions that would be most important to prevent complications while administering heparin. Provide a rationale for each intervention. 

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. 

Determine a patient s relative risk (low, moderate, high, or very high) of developing venous thrombosis. 

The prototype of this class is hirudin, which was originally isolated from the salivary glands of the medicinal leech, Hirudo medicinalis. Hirudin itself is not commercially available, but recombinant technology has permitted production of hirudin derivatives, namely lepirudin and desirudin.29,38,41 Lepirudin has a short half-life of approximately 40 minutes after IV administration and 120 minutes when given SC. Elimination of lepirudin is primarily renal therefore, doses must be adjusted based on the patient s renal function. The dose should be monitored and adjusted to achieve an aPTT ratio of 1.5 to 2.5 times the baseline measurement. Lepirudin is currently approved for use in patients with HIT and related thrombosis. Up to 40% of patients treated with lepirudin will develop antibodies to the drug.29,38,41... 

Pulmonary hypertension develops late in the course of COPD, usually after the development of severe hypoxemia. It is the most common cardiovascular complication of COPD and can result in cor pulmonale, or right-sided heart failure. Hypoxemia plays the primary role in the development of pulmonary hypertension by causing vasoconstriction of the pulmonary arteries and by promoting vessel wall remodeling. Destruction of the pulmonary capillary bed by emphysema further contributes by increasing the pressure required to perfuse the pulmonary vascular bed. Cor pulmonale is associated with venous stasis and thrombosis that may result in pulmonary embolism. Another important systemic effect is the progressive loss of skeletal muscle mass, which contributes to exercise limitations and declining health status. 

In chimpanzees, administration of Fab fragments of a monoclonal anti-F-VII antibody preceding an endotoxin bolus injection effectively blocked the activation of the coagulation pathway (B25). Administration of monoclonal anti-lL-6 under the same experimental conditions attenuated the activation of coagulation, while the fibrinolytic system remained unaltered. However, administration of monoclonal anti-TNF enhanced the tendency to microvascular thrombosis (P17,18). Monoclonal anti-TF antibodies administered to baboons as a pretreatment attenuated coagulopathy after induction of E. coli sepsis in these animals (T4). Primates pretreated with anti-C5a antibodies before infusion of E. coli developed less hypotension and had better survival rates than untreated animals, who developed ARDS and septic shock with a mortality rate of 75% (S35, Z6). No favorable treatment results have been published yet with one of these treatment modalities given to humans. 

Platelets play a role in each of the mechanisms of normal hemostasis vasoconstriction, formation of the platelet plug, and blood coagulation. However, they are also involved in pathological processes that lead to atherosclerosis and thrombosis (formation of a blood clot within the vascular system). Antiplatelet drugs interfere with platelet function and are used to prevent the development of atherosclerosis and formation of arterial thrombi. 

Radomski et al. [113] demonstrated that the CNTs were efficient in causing platelet aggregation both in vitro and in vivo, accelerating significantly the rate of development of carotid artery thrombosis in rats. Platelet aggregation was likely to result from MMP-dependent activation of GPIIb/IIa receptor. 

Various antibody preparations have been developed that facilitate imaging of vascular-related conditions, including myocardial infarction, deep vein thrombosis and atherosclerosis. Anti-myosin monoclonal antibody fragments (Fab) labelled with mIn, for example, have been used for imaging purposes in conjunction with a planar gamma camera. The antibody displays specificity for intracellular cardiac myosin, which is exposed only upon death of heart muscle tissue induced by a myocardial infarction (heart attack). 

Patients should be monitored for resolution of symptoms, the development of recurrent thrombosis, and symptoms of the postthrombotic syndrome, as well as for adverse effects from the treatments described in this chapter. 

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. 

The use of BRMs to treat human disease has its origins in the use of bacterial toxins to treat cancer by William B. Coley.73 These early studies resulted in the use of microbi-ally-derived substances such as BCG, Picibanil, carbohydrates from plants or fungi such as Krestin and Lentinan, other products such as Biostim and Broncho-Vaxom, as well as thymic extracts (Table 9.4). However, the lot-to-lot variation in the manufacture of these drugs has dampened enthusiasm. Equally, the focus on MOAs in drug development strategies has also dampened developmental efforts. The particulate nature of some BRMs can also result in pulmonary thrombosis and respiratory distress following i.v. injection. However, BRMs are commonly used to treat bladder cancer and derivatives of natural products are routinely used clinically. 

The plasma level of fatty acids in a fed subject is between 0.3 and 0.5 mmol/L. As discussed above, the maximal safe level is about 2 mmol/L. This is not usually exceeded in any physiological condition since, above this concentration, that of the free (not complexed with albumin) fatty acids in the blood increases markedly. This can then lead to the formation of fatty acid micelles which can damage cell membranes the damage can cause aggregation of platelets and interfere with electrical conduction in heart muscle (Chapter 22). The cells particularly at risk are the endothelial cells of arteries and arterioles, since they are directly exposed to the micelles, possibly for long periods of time. Two important roles of endothelial cells are control of the diameter of arterioles of the vascular system and control of blood clotting (Chapter 22). Damage to endothelial cells could be sufficiently severe to interfere with these functions i.e. the arterioles could constrict, and the risk of thrombosis increases. Both of these could contribute to the development of a heart attack (Chapter 22) (Box 7.4). 

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