5-hydroxytryptamine type 3 (5-HT3) receptor antagonists are used in the prevention of chemotherapy- induced, radiation-induced and postoperative nausea and vomiting. CYP2D6 polymorphisms can influence the metabolism of some of these drugs (i.e. ondansetron and tropisetron) thereby affecting drug efficacy. We summarize evidence from the published literature supporting these associations and provide therapeutic recommendations for ondansetron and tropisetron based on CYP2D6 genotype (updates at www.pharmgkb.org).
The continuum theory of anisotropic fluids, as developed by Ericksen and others, has been used to formulate an expression for the time derivative of the end-to-end vector of a linear macromolecule. When this expression is used in conjunction with the equation describing the distribution function for a dilute solution of dumbbell elements, the results exhibit important differences from the usual dumbbell theory. Presence of an additional term in the differential equation for the distribution function leads to the prediction of both a non-Newtonian viscosity and nonzero first and second normal stress differences in simple shearing flow. The normal stress differences are found to be of opposite sign, the secondary normal stress difference being negative. In small-amplitude oscillatory shear flow, and in pure deformational flow, the results are equivalent to those of the dumbbell theory. Expressions are presented for both stress and optical properties in an arbitrary homogeneous shear field.
Venous thromboembolism (VTE) is a significant problem in the perioperative period, increasing patient morbidity, mortality, and health care costs. It is also considered the most preventable of the major postoperative complications. Despite widespread adoption of prophylaxis guidelines, it appears that morbidity from the disease has not substantially changed within the past 2 decades. It is becoming clear that current prophylaxis efforts are not sufficient. Using more potent anticoagulants may decrease the incidence of VTE, but increase the risk for bleeding and infection. Much has been learned about the pathophysiology of venous thrombogenesis in recent years. Beyond the "traditional coagulation cascade," which anticoagulants modulate, there is a growing appreciation for the roles of tissue factor, monocytes, neutrophils, neutrophil extracellular traps, microvesicles, and platelets in thrombus initiation and propagation. These recent studies explain to some degree why aspirin appears to be remarkably effective in preventing thrombus propagation. Endothelial dysfunction, traditionally thought of as a risk factor for arterial thrombosis, plays an important role within the cusps of venous valves, a unique environment where the majority of venous thrombi originate. This suggests a role for newer treatment modalities such as statins. Not all patients have an equal likelihood of experiencing a VTE, even when undergoing high-risk procedures, and better tools are required to accurately predict VTE risk. Only then will we be able to effectively individualize prophylaxis by balancing the risks for VTE against the risks associated with treatment. Given the different cell types and pathways involved in thrombogenesis, it is likely that multimodal treatment regimens will be more effective, enabling the use of lower and safer doses of hemostatic modulating therapies such as anticoagulants, antithrombotics, and antiplatelet medications.
The identification in a patient of 1 of the 50 variants in the RYR1 or CACNA1S genes reviewed here should lead to a presumption of malignant hyperthermia susceptibility (MHS). MHS can lead to life‐threatening reactions to potent volatile anesthetic agents or succinylcholine. We summarize evidence from the literature supporting this association and provide therapeutic recommendations for the use of these agents in patients with these RYR1 or CACNA1S variants (updates at https://cpicpgx.org/guidelines and http://www.pharmgkb.org).
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