9/23/2023 0 Comments Fluid retention and heart failure![]() Therapeutic agents such as insulin, sulfonylureas, and meglitinides target primarily insulin availability. 1) suggests that appropriate treatment should target both the insulin resistance and the inadequate insulin secretion. This formulation of insulin-resistant T2D as two interacting pathophysiologic entities (Fig. These and other data suggest that the metabolic syndrome is the driving factor in the development of cardiovascular disease and that hyperglycemia is a factor that exaggerates cardiovascular disease in the metabolic syndrome setting. Patients with no diabetes and the metabolic syndrome had a 13.9% prevalence of coronary heart disease and those with diabetes and the metabolic syndrome had a 19.2% prevalence of coronary heart disease. Data from NHANES III participants 50 years or older showed that patients with T2D and no metabolic syndrome had a prevalence of coronary heart disease of 7.5% which did not differ from a non-diabetic population with no metabolic syndrome (prevalence 8.7%). Patients with T2D may have hyperglycemia and no metabolic syndrome (up to 15% of patients with T2D) or hyperglycemia with the metabolic syndrome (85% of patients with T2D). Insulin resistance increases the prevalence of T2D sixfold as marginal insulin secretion becomes inadequate insulin secretion. The metabolic syndrome results in increases in atherosclerotic diseases, hepatic steatosis and steato-hepatitis, and hypertension. ![]() These ectopic increases in lipids define the metabolic syndrome. While a few investigators suggest that hyperinsulinemia itself may be a primary cause of insulin resistance, the overwhelming data indicate that insulin resistance is a primary defect due to abnormalities in the distribution of adipose tissue products in hepatic and extrahepatic tissues. In contrast, when insulin action is impaired (insulin resistance), hyperglycemia occurs when insulin secretion is inadequate to overcome the insulin resistance. Thus, when insulin action is normal, hyperglycemia occurs when absolute insulin secretion is deficient. This conflict has been resolved in that hyperglycemia only occurs when insulin secretion is insufficient to overcome barriers to insulin action. Moreover, it also serves as a reference textbook for medical students, residents and fellows dealing in everyday practice with fluid overloaded and oliguric patients.For years there was an intense debate as to whether the primary defect in type 2 diabetes (T2D) was insulin resistance or insulin secretory deficiency. Clearly structured and written, the present book is a practical tool for physicians and professionals involved in the management and care of patients with combined heart and kidney disorders. Subsequently, different conditions leading to fluid overload are described, followed by an account of emerging diagnostic tools, therapies and technologies devoted to the treatment of patients with severe fluid-related disorders. In the first section, the authors present new definitions for heart failure, acute kidney injury and cardiorenal syndromes to facilitate the process of understanding the complex link between the heart and the kidney. The present publication is divided into four parts: Definition and Classification, Pathophysiology, Diagnosis and Therapy. A thorough assessment of the fluid status of the patient may help guide the therapy and prevent complications induced by inappropriate therapeutic strategies. Fluid overload is often observed in patients with heart failure and secondary oliguric states.
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