Home Remedies for Hyperglycemia

Blood Sugar Miracle

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Several studies have demonstrated the link between elevated HbA1c plasma levels and CV risk. A multi-variate analysis of the United Kingdom Prospective Diabetes Study (UKPDS) study involving 2693 diabetic patients without known CV disease demonstrated that, for each increment of 1 in HbA1c at baseline, the CV risk increased independently by approximately 10 over a median follow-up of 8 years. Although hyperglycemia has been associated with CVD and epidemiologic evidence links lower blood glucose levels to a decrease in CV events, aggressive blood glucose control in type 2 diabetes within randomized trials has not been shown to significantly reduce macrovascular events,129 with the exception of patients presenting with acute MI105 or undergoing CABG.67 On the other hand, aggressive glucose-lowering therapy was associated with a significant reduction in microvascular complications.129 A putative explanation for the observed lack of benefit of glucose-lowering therapies on macrovascu-lar...

Multifactorial Intervention

The Steno-2 study compared the efficacy of a targeted, intensified, multifactorial intervention with that of conventional treatment on modifiable risk factors for CV disease in 160 patients with diabetes and microalbuminuria.140 The primary end point was a composite of CV death, nonfatal MI, stroke, revas-cularization, and amputation. Intensive treatment was characterized by a stepwise implementation of behavior modification and pharmacologic therapy that targeted hyperglycemia, hypertension, dyslipid-emia, and microalbuminuria, along with secondary CV prevention with aspirin. Conventional treatment was in accordance with national guidelines. After a mean follow-up of 8 years, patients receiving intensive therapy had a significantly lower risk of CVD (HR 0.47), nephropathy (HR 0.39), retinopathy (HR 0.42), and autonomic neuropathy (HR 0.37). The authors concluded that a target-driven, long-term, intensified intervention aimed at multiple risk

To Artificially Sweeten or

People often have to use artificial sweeteners because of a medical condition. For example, sugar substitutes can be great for diabetics, who can't tolerate real sugar because their bodies can't produce the hormone insulin. Insulin delivers the sugar from our blood to our cells, where we utilize it as energy. When your body doesn't have enough insulin, sugar builds up in the blood and doesn't get into the cells. This condition is known as high blood-sugar and can be extremely dangerous for people with diabetes. Because sugar substitutes do not contain any glucose (and therefore do not require insulin), they can be effective sweeteners for people with diabetes.

Patient Encounter Part 2

Patients with mild CFRD may be managed with carbohydrate modification if their nutritional status is optimal. However, most patients present with poor nutrition and weight loss and require more aggressive treatment. Because CFRD results from insulin insufficiency, exogenous insulin replacement is usually required. Many patients can be successfully managed by meal coverage with short- or rapid-acting insulin (regular, lispro, or aspart) dosed per carbohydrate counting. Patients with fasting hyperglycemia or patients receiving nighttime tube feedings typically also require longer-acting basal insulin. Regular home glucose monitoring is essential to appropriate therapy. Little information is available regarding use of oral antidiabetic agents in CFRD, and routine use is not recommended. ,8

Testosterone effects on fat metabolism

Percent body fat is higher in hypogonadal men in comparison to eugonadal controls (Katznelson etal. 1998). Induction of androgen deficiency in healthy men by administration of a GnRH agonist leads to an increase in fat mass (Mauras et al. 1998). Some studies of young, hypogonadal men have reported a decrease in fat mass with testosterone replacement therapy (Brodsky etal. 1996 Katznelson etal. 1996 Snyder etal. 2000) while others (Bhasin etal. 1997 Wang etal. 1996) found no change. In contrast, long-term studies of testosterone supplementation of older men have consistently demonstrated a decrease in fat mass (Kenny etal. 2001 Snyder etal. 1999 Tenover 2000). Epidemiologic studies (Khaw and Barrett-Connor 1992 Seidell etal. 1990) have shown that serum testosterone levels are lower in middle-aged men with visceral obesity. Serum testosterone levels correlate inversely with visceral fat area and directly with plasma HDL levels. Testosterone replacement of middle-aged men with visceral...

Infant of a Diabetic Mother

The risk of RDS in an IDM is five to six times greater than in the infant of the nondiabetic mother before 38 weeks' gestation. Animal studies have implicated hyperglycemia and hyperinsulinemia within the uterine environment as causing the delay of pulmonary maturation (Tyrala, 1996). Lung maturation studies (e.g., lecithin sphingomyelin ratio by amniocentesis) should be considered before an elective cesarean section in a diabetic mother. Poor blood sugar control during the early weeks of pregnancy can result in a fourfold to eightfold increase in congenital malformations, such as cardiac defects and CNS anomalies. The higher the hemoglobin A1c, the greater is the incidence of congenital anomalies (Tyrala, 1996). There are no anomalies that are found only in the offspring of diabetic women. The most common cardiac malformations include transposition of the great vessels, ventricular septal defect, coarctation of the aorta, hypoplastic left ventricle, and pulmonic stenosis. CNS...

Clinical Manifestations

First stage susceptibility based on a combination of (1) genetic risk factors (2) physiological states such as obesity for type II diabetes (3) and environmental factors including diet, climate, activity, and other life-style patterns. Second stage glucose intolerance, which is recognized as a phase preceding both insulin-dependent and non-insulin-dependent diabetes. Not all individuals having impaired glucose tolerance progress to symptomatic diabetes. Third stage chronic hyperglycemia without complications.

History and Geography

Dicate that we may anticipate an increase in the worldwide prevalence of DM. The focus has been and remains on treatment of hyperglycemia and the vascular complications of long-term diabetes. Using the epidemiological data and historical perspectives, we are now beginning to develop better programs aimed at early intervention and prevention.

Nonsteroidal Anti Inflammatory Drugs

Low-dose glucocorticoid treatment (equivalent to prednisone 10 mg day or less) effectively reduces inflammation through inhibition of cytokines and inflammatory mediators and prevents disease progression.19,21 The goal of glucocorticoid use is to minimize adverse drug events by keeping doses low and using the drugs as infrequently as possible. Patients may receive glucocorticoids for a brief time as bridge therapy following DMARD initiation or via intra-articular injections to relieve symptoms of active disease. Patients taking more than 10 mg day prednisone or equivalent are at an increased risk for clinically significant adverse reactions, especially bone loss leading to osteoporosis. Other glucocorticoid-related adverse reactions include Cushing's syndrome, peptic ulcer disease, hypertension, weight gain, infection, mood changes, cataracts, dyslipidemia, and hyperglycemia.

Vitamins and Minerals

While there's nothing wrong with taking a daily multivitamin, megadoses aren't a good idea because their long-term safety remains in question. Over the years, various supplements have been recommended for an assortment of ailments. B-vitamins, for instance, were used to treat diabetic neuropathy, but their beneficial role was never proven and they're not recommended as a therapeutic option. Although chromium piccolinate was reported to have a good effect on blood-sugar control, it was never conclusively demonstrated. One antioxidant, alphalipoic acid, is a prescription drug in Germany that has been used to treat diabetic neuropathy. Although studies are underway in the United States, results will not be available for years.

Dyslipidemia Hypertension and Atherosclerosis

The unexpectedly negative outcomes of diabetic studies targeting hyperglycemia as a cardinal risk factor for progression of atherosclerosis emphasize the need to correct dyslipidemia and hypertension typical of the type 2 diabetic state. Dyslip-idemia occurs chiefly when beta cells are unable to maintain the high insulin levels required to inhibit lipolysis from adipose cells. The resulting free fatty acidemia associated with high insulin levels causes the liver to repackage these energy substrates into more triglyceride-rich lipoproteins.

Pathogenesis and Presentation

Diabetic ketoacidosis (DKA) results when an absolute or relative lack of insulin allows hyperglycemia to become dehydrating and lipolysis to become ketosis. This progression occurs over several days in patients who are usually unaware of their DM diagnosis. As dehydration becomes more severe, the brain begins to experience an increase in osmolality. Altered mental status begins with lethargy and coincident metabolic acidosis. The patient may become dependent on others to secure medical care if care is further delayed, lethargy becomes stupor and eventually coma. The pH falls to 7.00 or lower. The crisis has been defined.

Diabetic Macroangiopathy Accelerated Atherosclerosis

The mechanisms causing accelerated atherosclerosis in DM are linked to the lipid and inflammatory pathogenic paradigms. Lipid abnormalities are not as common in type 1 patients, but long-term follow-up of the DCCT cohorts found thickening of large blood vessels related to their history of diabetic control. The disturbances in fatty acid metabolism in type 2 patients result in common dyslipidemias implicated in development of atherosclerotic plaque. Insulin resistance is associated with lipoprotein and coagulation abnormalities, hypertension, and evidence of endothelial dysfunction, all of which contribute to atherogenesis, even before the onset of hyperglycemia. These associations suggest that type 2 diabetes occurring as insulin levels decline is only one component of a larger pathophysiologic process.

Blood glucose see Chapter

Measurement of blood glucose is mandatory for all patients with suspected stroke. Hypoglycemia (serum glucose < 2.8 mmol l) with consequent neuroglyco-penia is an important stroke mimic and is readily corrected by the intravenous infusion of 10-20 dextrose 1 . Hyperglycemia has a reported prevalence of up to 68 of acute stroke admission, and is not restricted to those patients with previously diagnosed diabetes mellitus 41 . The prevalence of previously unrecognized diabetes mellitus or impaired glucose tolerance may be between 20 and 30 42 . There is evidence of a positive association between elevated admission plasma glucose and poor post-stroke outcome, with increasing stroke severity, higher mortality and reduced functional recovery observed in those with hyperglycemia 41, 43 . Tight control of hyper-glycemia following myocardial infarction and in critically ill patients being managed in intensive care units appears to confer a beneficial outcome, and so it has been suggested...

Recommendation for Tuna

Gestational diabetes is the onset of high blood sugar (or carbohydrate intolerance) that is generally detected around the twenty-eighth week of pregnancy. Because this condition is caused by the placenta putting out large doses of anti-insulin hormones, as soon as the placenta is removed (during the baby's delivery), the condition disappears in almost all cases. Women diagnosed with gestational diabetes have very specific dietary concerns and should work with a qualified nutritionist (registered dietitian) on appropriate meal planning.

Endocrine Pancreas and Stress

Another important role of the endocrine pancreas is its involvement in the hyperglycemia that accompanies various kinds of stress. A few examples of stress are illustrated. During physical exercise, there is an increased hepatic glucose output, which underlies the hyperglycemia, as a result of increased activity in the sympathetic nerves and elevated arterial epinephrine levels.167 Accompanying these changes is an inhibition of insulin secretion and a stimulation of glucagon secretion, which exaggerate the hepatic glucose output and also reduce the peripheral glucose uptake. This optimizes the availability of glucose to the central nervous system during stress. A system for studying the mechanisms of these influences was previously introduced in the swimming mouse model, in which standardized 2-minute swimming is An important factor for the restoration of blood volume during bleeding is an increase in the plasma glucose level, which induces osmotic absorption of fluid into the blood...

Perioperative Management of the Diabetic Surgical Patient

In patients with T1DM, withholding insulin leads to the development of ketosis, adding to the nutritional and electrolyte problems that often accompany surgical illness. In these individuals, it is important to provide a certain amount of insulin at all times, even during fasting. This is most easily done with the IV coadministration of 5 dextrose in water (100 to 200 mL hr) and R insulin (1 to 2 units hr) begun the evening before surgery. Ambient blood levels are maintained between 100 and 150 mg dL. Blood glucose is monitored every 1 to 2 hours before surgery and hourly during surgical anesthesia to optimize metabolic control. More commonly used methods, such as providing one half to two thirds of the usual intermediate insulin dose on the morning of surgery, may be adequate. However, this method results in a peak of insulin action, which will not necessarily coincide with a planned meal. In addition, insulin absorption from SC tissues may be altered during surgery because of...

Glucose Metabolism Disorders Hypoglycemia

Hypoglycemia is associated with a substantial morbidity, primarily related to accidents (e.g., vehicular) and seizures with resultant injuries. y In the setting of hypoxic encephalopathy, premature prognostication should be avoided, given that slow improvement may continue for 1 to 2 years.y When glucose is replaced before the medullary phase is reached, the features may be reversible. After this point, especially if treatment was delayed, recovery may be protracted or incomplete. y The potential risk of glucose administration to euglycemic and hyperglycemic patients is small compared with the potentially substantial benefit. However, the possibility of cerebral ischemia must be considered, because hyperglycemia at the onset of brain ischemia worsens the postischemic outcome, whereas hyperglycemia occurring after experimental cerebral infarction does not. y , '117 HYPERGLYCEMIA Pathogenesis and Pathophysiology. Although the brain tolerates...

Degenerative Unverricht Lundborg

In adult patients, the most common type of SE is secondary generalized convulsive SE (GCSE). Generalized convulsive SE is characterized by intermittent or continuous overt convulsive activity accompanied by coma and epileptiform activity on EEG. The manifestations change over time such that discrete convulsions give way to increasingly subtle clinical manifestations, which is a condition known as subtle SE. Eventually, electrical status without clinical manifestations is all that remains. Occasionally, subtle SE occurs without prior convulsive activity in patients with severe diffuse cerebral dysfunction. Generalized convulsive activity produces various systemic effects including hypoxia, hyperpyrexia, blood pressure instability, and cerebral dysautoregulation. Metabolic derangements including respiratory and metabolic acidosis hyperazotemia hypokalemia hyponatremia hyperglycemia followed by hypoglycemia and marked elevations of plasma prolactin, glucagon, growth hormone, and...

Metabolic Complications

Metabolic complications of EN most commonly include disorders of fluid and electrolyte homeostasis and hyperglycemia. More severely ill patients require more frequent monitoring (see Table 101-9). Both dehydration and fluid overload can occur with tube feeding. Careful monitoring of fluid inputs and outputs as well as body weight is important. Dehydration may be due either to excessive fluid losses or inadequate fluid intake. The trend in the BUN-to-serum-creatinine ratio can be useful in helping monitor for this complication a ratio of greater than about 15 1 may be an indicator of dehydration. Attention should be paid to the free-water content of EN formulas this information usually is included on product labeling. Free-water content of EN formulas varies from about 65 to 85 , with percentage of free water typically dropping as caloric density of the formula rises. If dehydration develops, switching to a less calor-ically dense formula or using more water flushes may be appropriate....

Appropriate Antidiabetic Protocols

The family physician must determine if it is appropriate to continue the outpatient treatment schedule in the hospitalized diabetic patient, depending mainly on the reason for hospitalization. If the patient can eat, the regular outpatient treatment (oral agents and or insulin) should be continued with appropriate adjustments. Supplementing this with basal bolus insulin may be appropriate if significant hyper-glycemia (> 200 mg dL) occurs associated with the stress of illness and hospitalization. The outpatient regimen should not be discontinued in favor of a fixed sliding-scale insulin schedule, which will take days to titrate to the patient's needs and may result in erratic hyper- and hypoglycemic intervals. If the patient cannot be fed and glucose values are drifting above the 150- to 180-mg dL range because of stress-mediated gluconeogenesis, treatment to prevent further hypergly-cemia is appropriate.

Pericytes and Disease

Pericyte loss or a reduced pericyte to EC ratio may be achieved through migration of pericytes from their microvascu-lar location under pathological or physiological conditions, selective pericyte death or from reduced pericyte turnover or maintenance. Pericytes migrate naturally during the early phases of physiological angiogenesis to make way for growing sprouts (113, 114), or in response to stress or injury (21). Migration following TBI is thought to promote survival as pericytes remaining in their vascular location show signs of degenerative activity (21). However, migration is also thought to play a pathogenic role in diabetic retinopathy (115). Decreased pericyte to EC ratios have been observed following TBI (21) and stroke (116), multiple sclerosis (117-121), brain tumor (122, 123), diabetic retinopathy (124), aging (125, 126), and in a variety of angiopathies (127). Pericyte loss may also play a role in Alzheimer's disease, however enhanced pericyte coverage of some vessels...

Structure and Physiology

Accidentes Vivo Pulidores

There is decreased metabolism of thyroxine and decreased conversion of thyroxine to triiodo-thyronine. Because of a reduction in pancreatic beta cell secretion, hyperglycemia may result. The hypothalamus and the pituitary gland secrete reduced amounts of hormones. An increase in the secretion of antidiuretic hormone and atrial natriuretic hormone may alter fluid balance. There are also increased levels of norepinephrine.

Preoperative Evaluation and Preparation

Symptomatic patients with functional tumors require correction of fluid and metabolic abnormalities (e.g., hypokalemia, metabolic alkalosis, and hyperglycemia) and control of hypertension and other symptoms related to hormone excess. Patients with Cushing's syndrome can be treated with ketokenazole or the antiglucocorticoid agent RU 486. Postoperatively, these patients require glucocorticoid replacement to avoid postoperative adrenal insufficiency. Patients with hyperaldosteronism are treated with spironolactone. Patients with pheochromocytoma are managed with fluids, a blockade and, if necessary, (3 blockade. Finally, in patients with suspected malignancy, a thorough evaluation for metastatic disease should be undertaken.

Emergency surgery and diabetic ketoacidosis

Diabetics who require emergency surgery often have a grossly elevated blood glucose concentration and occasionally overt ketoacidosis. Such patients require rehydration, correction of sodium depletion, correction of subsequent potassium depletion and i.v. soluble (Humulin S) insulin by infusion at an initial rate of 4-8 unit h l.

Nox Family of Nadph Oxidases

NADPH oxidases are activated by diverse stimuli such as angiotensin II, proinflammatory cytokines, vasoconstrictors, hypoxia, growth factors, metabolic factors (hyperglycemia, hyperinsulinemia, free fatty acids, advanced glycation end products AGEs ), mechanical stimuli, and superoxide itself. The NADPH oxidase-derived ROS have been implicated in aging and a variety of diseases, including hypertension, diabetes mellitus, hypercholesterolemia, hypertension, and SCD 19 . In recent years, emerging evidence suggests a role of NADPH oxidase in several ED states, as discussed later in this chapter.

Rationale for Targeting VEGF

Angiogenesis Foundation

Angiogenesis - the growth of new blood vessels - is a central component of many human disease processes (Witmer et al., 2003). There are several examples that have been areas of very active research. As solid tumors grow they require an ever-increasing supply of oxygen and nutrients, and hence develop their own vascular beds in order to meet this requirement. In patients with diabetes mellitus, chronically elevated blood glucose levels result in damage to small blood vessels and resultant end-organ ischemia distal to these sites of damage. Subsequently compensatory vascular beds adjacent to these sites of damage emerge in an effort to maintain tissue perfusion. In neovascular AMD, tufts of neovascular tissue grow from the choroid underlying the macula (the central portion of the retina) in response to metabolic distress. These neovascular tufts leak fluid and bleed, leading to loss of central vision.

Niacin and Nicotinic Acid

Superphysiological doses of niacin (1.5 to 3 g daily) have been used successfully in the treatment of hypercholesterolemia, and this practice diminishes mortality by reducing a coronary artery disease risk factor. Side effects of high-dose niacin include flushing, hyperuricemia, hyperglycemia, and elevations in liver enzymes.

Polymotor Sensory Neuropathy

In the early phase of diabetic neuropathy, physical examination may be uninformative. Assessing the adequacy of perfusion is critical and easily accomplished by inspecting the toenails for capillary perfusion and palpating the tibialis posterior and dorsalis pedis arteries. As noted, a dry, cool foot with thickened or thin subcutaneous tissue and nonelastic skin is demonstrating microangiopathy, despite a palpable dorsalis pedis, indicating a likely positive result in decreased deep tendon reflexes at the ankle, vibratory sensation, position sense, hot-cold discrimination, or fine touch with monofilament test. Inability to perceive the monofilament indicates advanced neuropathy that would endanger the foot if injured. Peripheral neuropathic symptoms may also result from hyperglycemia-mediated nerve injury with no clinical evidence of loss of capillary density. Over time, paresthesias and burning pains usually improve, unless functional factors (endogenous or related to narcotic...

Table 461 Overview Of The Neuroendocrine Stress Response

After surgical insult includes a general increase in catabolic hormones, such as catecholamines, Cortisol, renin, aldosterone, and glucagon, which result in hyperglycemia, muscle protein catabolism (negative nitrogen balance), and increased lipolysis. In addition, there is sodium and water retention, with a shift of extracellular fluid to intracellular compartments.1 A general decrease in immune function and activation of coagulation are also associated with the stress response. The net result is a hypermetabolic, catabolic state resembling semistarvation. Although data with regard to the stress response effect on patient outcomes are inconclusive, there are many detrimental consequences of prolonged surgical stress. Catecholamine release causes increases in heart rate, which may result in postoperative myocardial ischemia or infarction. Hyperglycemia and insulin resistance may contribute to poor wound healing and depression of immune function.113 Negative nitrogen balance and protein...

General Characteristics

The foregoing data indicate that we may anticipate an increase in the worldwide prevalence of DM. The focus has been and remains on treatment of hyperglycemia and the vascular complications of long-term diabetes. Using epidemiological data and historical perspectives, we are beginning to develop better programs aimed at early intervention and prevention.

Preconception Counseling

During pregnancy, maternal illness can adversely affect the fetus and lead to adverse neonatal outcomes. Maternal hypertension, preeclampsia, alcohol and tobacco use, illicit drug use, and autoimmune diseases can cause intrauterine growth restriction (IUGR) and preterm birth. Children born to women with diabetes mellitus or gestational diabetes are at risk for shoulder dystocia, operative delivery, hypoglycemia, and birth trauma (American College of Obstetricians and Gynecologists ACOG , 2005). Maternal hyperglycemia at delivery also puts the infant at risk for hypoglycemia. Poorly controlled maternal hypothyroidism and hyperthyroidism are associated with low birth weight (LBW) and preterm delivery (ACOG, 2005). Fetal alcohol syndrome is directly caused by maternal alcohol use and abuse, and other illicit drug use is associated with preterm birth, congenital abnormalities, neurobehavioral abnormalities, and neonatal drug withdrawal syndromes (ACOG, 2005). Box 22-1 lists the more...

Definition and Pathogenesis

Diabetes mellitus is currently defined as a group of metabolic disorders characterized by hyperglycemia that result from defects in the secretion and action of insulin. Normally, plasma glucose, the primary substrate for brain function, is tightly regulated within a narrow fasting range of 60 to 100 mg dL by insulin secreted from the beta cells of the pancreatic islets. Daily mean glucose values which exceed 100 mg dL have been associated with the progression of diabetic complication. Over the long term, diabetic patients often develop complications such as retinopathy, neuropathy, nephropathy, and accelerated aging of the cardiovascular system. mellitus (DM), the metabolic errors of diabetes are likely disordering the utilization of all substrates long before hyperglycemia becomes apparent. Both glucose and fatty acids are energy substrates oxidized by muscles, including the myocardium, for adenosine triphosphate (ATP) generation. The relative lack of insulin in DM leads to lipolysis...

Regional and General Anesthesia and Surgical Stress

Of certain stress hormones, like adrenaline and Cortisol, by the adrenal gland. These hormones can be detrimental to the body in a great number of ways when they persist for extended periods. The release of adrenaline alone increases heart rate, blood pressure, and oxygen demands on the heart, which may be harmful or fatal in the patient with advanced heart disease. It also causes elevated blood glucose levels and can impair the immune response, increasing susceptibility to infection.

Honorio T Benzon Adrienne E Knight

Trauma is tissue damage caused by an extrinsic force.13 The stress response to trauma and the accompanying pain activate neurohumoral and physiologic processes ( Table 26-1 ). These responses result in hyperglycemia, lipolysis, protein catabolism, increased catecholamine and antidiuretic hormone levels, a hypercoagulable state, and immunosuppression. hj Trauma has direct and reflex-related effects on the cardiovascular, pulmonary, gastrointestinal, renal, musculoskeletal, and immunologic systems. Clinically, there is tachycardia and hypertension. Thoracic and abdominal injuries cause chest splinting, reflex-activated diaphragmatic dysfunction, hypoventilation, atelectasis, ventilation perfusion mismatch, and hypoxia. Vital capacity and the functional residual capacity decrease, coughing is impaired, secretions are retained, and secondary pneumonia develops. Immobility may result in deep venous thrombosis and possible pulmonary embolism. There is increased sympathetic tone, decreased...

Critical illness trauma and surgery

Critical illness, trauma, burns, surgery and malnutrition all result in a catabolic state characterised by acute muscle breakdown which is reversed during recovery. These catabolic states are characteristically accompanied by functional hypogo-nadotrophic, androgen deficiency. This is due to functional partial GnRH deficiency as pulsatile GnRH administration can rescue LH pulsatility and hypoandrogenemia (Aloi et al. 1997 van den Berghe et al. 2001). This has long led to the hypothesis that androgen therapy might improve mortality or morbidity by pharmacologically enhancing nutritional supplementation and muscle, bone and skin recovery. However, the endocrine response to catabolic states such as critical illness are highly complex involving widespread dysregulation of all pituitary hormonal axes (Van den Berghe 2003) so that restoration of individual anabolic hormones may be inadequate. Nevertheless the success of intensive insulin therapy to regulate hyperglycemia (van den Berghe et...

Infectious Complications

Patients receiving central PN are at increased risk of developing infectious complications caused by bacterial and fungal pathogens.1,50 Infections may be related to placement of a central venous catheter, contamination of a central venous catheter or IV site (catheter-related infection), and persistent hyperglycemia. Strict aseptic techniques must be used when placing the catheter, along with continuous care of the catheter and infusion site. Catheter-related bloodstream infections are a common complication in long-term PN patients, often requiring hospital admission for parenteral antimicrobial therapy and or removal of the catheter. Contamination of the PN admixture is possible, although rare if protocols are followed for aseptic preparation of PN admixtures. Lack of use of the intestinal tract also may increase the risk of infection possibly by reducing gut immunity, leading to intestinal bacterial overgrowth and subsequent systemic bacterial translocation.

Enteral Versus Parenteral Feeding

With the advent of the technique of PN by a large central vein in the late 1960s, this modality of feeding quickly became popular. PN was used originally in patients with-inflammatory bowel disease (IBD) or congenital bowel abnormalities but was incorporated quickly into care of other types of patients such as the critically ill. The relative ease of PN administration, along with the perception that critically ill patients had prolonged high-energy expenditures, led to complications of overfeeding. In the United States, where no IV fat emulsion was available commercially for several years during the 1970s, the impact of dextrose overfeeding was observed. Complications included hyperglycemia, carbon dioxide overproduction leading to delays in weaning from mechanical ventilation, and liver abnormalities owing to hepatic steatosis. perglycemia occur easily with PN administration, and the potential harm of hyper-glycemia, especially in critical-care populations, has been demonstrated...

Heart Failure and Diabetic Cardiomyopathy

Of diabetic patients after exclusion of left ventricular hypertrophy or ischemia.32 In the 1970s, the observation that diabetic patients may suffer from congestive heart failure in the absence of hypertension, CAD, or other evident source of cardiac disease led to the concept of diabetic cardiomyopathy, also called diabetic heart disease. Although the exact mechanisms underlying the condition are unknown, the accumulation of extracellular matrix proteins, and in particular of collagen, appears to be a key biologic dysfunction (Fig. 2-4).33 The deposition may be the result of excess production, reduced degradation, and or chemical modification of extracellular matrix proteins. These processes are believed to be induced directly or indirectly by hyperglycemia. Fibrosis may be the result of both increased activity of angiotensin II receptors and increased levels of angiotensin II.

Endothelial Dysfunction

Diabetes vascular disease is characterized by endothelial dysfunction, a biologic abnormality that has been related to hyperglycemia, increased free fatty acid production, decreased bioavailability of endothelium-derived NO, formation of advanced glycation end products (AGE), altered lipoproteins, hypertension, and, as previously mentioned, insulin resistance.11 A decreased bioavailability of endothelium-derived NO, with subsequent impaired endo-thelium-dependent vasodilation, has been observed in diabetic individuals even before the development of detectable atherosclerosis. NO is a potent vasodilator and a key compound of the endothelium-medi-ated control mechanisms of vascular relaxation. In addition, it inhibits platelet activation, limits inflammation by reducing leukocyte adhesion to endothe-lium and migration into the vessel wall, and reduces vascular smooth muscle cell proliferation and migration. As a consequence, an intact NO metabolism in the vessel wall has a protective...

The Burden Of The Disease

The diagnostic criteria for diabetes recommended by the ADA are presented in Table 2-1. In the absence of unequivocal hyperglycemia, one of these criteria must be confirmed on a subsequent day to establish the diagnosis. Although the plasma level of hemoglobin A1c (HbA1c) reflects mean plasma glucose concentrations over the preceding 2 to 3 months, the use of this parameter for the diagnosis of diabetes is currently not recommended.7 Before the development of diabetes, subjects pass through a stage of impaired glucose metabolism characterized by impaired fasting glucose (IFG) levels or impaired glucose tolerance (IGT) (see Table 2-1). These two metabolic disturbances predispose to diabetes and CVD and were recently grouped in the term prediabetes. A cluster of lipid and non-lipid risk factors of metabolic origin mediated by insulin resistance, such as pathologic glucose metabolism, obesity, hypertension, and dyslipidemia, was designated the metabolic

Endocrine Pancreas and Type 2 Diabetes

However, in patients who proceed to type 2 diabetes, there is a defect in glucose action on the B cells, leading to impaired glucose-stimulated insulin secretion, making it impossible for the B cells to compensate fully for the peripheral insulin insensitivity. This leads to hyperglycemia and diabetes.19159 Hence, the main defect in type 2 diabetes is defective beta cells insulin resistance can be regarded as a risk factor because it may unmask the defective islet function. Also, the ability of the A cells to respond properly with inhibition of glucagon secretion when the glucose level is increased is impaired in diabetes.159 This leads to hyperglucagonemia, which, together with the insufficient hyperinsulinemia, increases the hepatic glucose output and reduces the glucose uptake in peripheral tissues, which are the metabolic signs of type 2 diabetes. Central to the disease is the inability of the B cells to respond normally to increased glucose levels. This may be due both to...

The Gut and Insulin Secretion

GLP-1 is the most important incretin hormone.103,106'107 This peptide is processed from proglucagon in the intestinal L cells and released into the blood during meal ingestion. GLP-1 potently stimulates insulin secretion at concentrations that are produced by food intake. The peptide has, in addition, been of interest as a potential novel treatment modality in diabetes because of its combined effect to stimulate insulin secretion, inhibit glucagon secretion, and reduce blood glucose levels by a peripheral effect.108 109 It should be recalled that GLP-1 is not produced in the pancreatic A cells but only in the intestinal L cells because of the cell-specific posttranslational modification of proglucagon related to differential expression of proconvertases. A problem in developing GLP-1 as a treatment for type 2 diabetes is that it is rapidly degraded by means of the enzyme dipep-tidyl peptidase IV (DPPIV).110 This enzyme is expressed in several tissues, including endothelial cells,...

Hospital Care of Diabetic Patients

Protocols with continuous insulin infusion are now being widely applied. Good glucose control in known diabetic patients and those with marked hyperglycemia and critical illness shortens intensive care unit (ICU) and respirator time and reduces associated polymyopathy while generally improving all outcome parameters. Many post-cardiothoracic surgery units have adopted these protocols to improve myocardial energetics, limit infection, and discharge the patient sooner.

Initiating Insulin for Type 2 Diabetes

The classic setting for the use of insulin is in a newly diagnosed type 1 diabetic patient. However, insulin is more frequently used in the treatment of type 2 diabetes to compensate for the secretory defect that often progresses to a profound loss of insulin secretory reserve. This is suggested when FSG or HbA1c continue to rise despite the patient's best behavioral efforts and multiple oral drugs. A patient with type 2 diabetes can also present late in its course with marked hyperglycemia and even ketosis. In these patients, insulin treatment protocols used in type 1 diabetes are appropriate until the type 2 pattern of glucose homeostasis is recognized. In most patients, convenience insulins such as human or synthetic 70 30 or 75 25 combinations can be used for several days until the effects of behavioral measures and oral agents kick in. Dosage is usually from 0.2 to 0.5 units (U) kg body weight day (in elderly patients, consider 0.1 U kg day). The initial dosage selected is a...

Maturity Onset Diabetes of Young

Genetic defects of beta-cell function involve genes coding for hepatic transcription factors and glucokinase. In the MODY variant, hyperglycemia is observed during childhood or adolescence and is caused by a diminution in beta-cell secretion without impairment in insulin action. The genetic disorders are autosomal dominant, and the glucokinase defect impairs the conversion of glucose to glucose-6-phosphate, which is involved in insulin secretion. This glucokinase dysfunction causes a loss of the beta-cell glucose sensor. The resulting diabetes is generally not prone to ketosis. Many patients with milder forms of diabetes treated as type 1 eventually are found to have similar genetic defects.

Insulindependent diabetes mellitus

Children with type 1 diabetes mellitus may, however, not only experience hypoglycemia with exercise. When insulin levels are insufficient, exercise may lead to ketoacidosis. Therefore, not only low but also high blood glucose levels may indicate possible risks of subsequent physical activities.

Revascularization In Diabetic Patients With Stable Coronary Disease

Whereas in-hospital and 30-day outcomes after PCI in diabetic patients are comparable to those of non-diabetics, large-scale registries have identified diabetes as an independent predictor of long-term mortality and need for repeat revascularization. Putative mechanisms negatively affecting outcomes may include endothelial dysfunction, prothrombotic state, greater propensity for restenosis and adverse vascular remodeling after angioplasty, increased protein glycosyl-ation, and vascular matrix deposition (see Fig. 2-2).9 All of these processes appear to be exacerbated by hyperglycemia and hyperinsulinemia. In addition, diabetic patients more frequently have noncar-diac comorbidities that may also negatively affect outcomes.

Image Diagnosis of Medullary Cancer

Metastatic tumors with minimal adverse effects.72 Also, in many other articles, no important adverse effect is mentioned.7378 However, in one article, a patient with metastatic pheochromocytoma to the lung, liver, and paraaortic lymph node was treated with 3.7 GBq (100 mCi) of 13II-MIBG. The metastatic nodes in the lung and liver disappeared, and the secretion of catecholamine levels decreased to normal. Major but temporary untoward responses were hypertension and hyperglycemia.79

Management of Acute Stroke

Regular determinations of blood glucose levels to avoid hyperglycemia NPO until there is certainty about the gag reflex pending swallowing evaluation Cerebral edema usually peaks within 2 to 4 days after a stroke. It is seldom a problem during the first 24 hours, except in cases of large cerebellar CVAs. Steroids are not used to treat cerebral edema related to thromboembolic strokes. Steroids are generally ineffective and may exacerbate hyper-glycemia and raise BP. Cerebral edema related to throm-boembolic stroke is first treated by raising the head of the bed 20 to 30 degrees. Hyperventilation can work rapidly to reduce intracranial pressure (ICP) but has only a transient effect. Mannitol can be given to lower ICP at 0.25 to 0.5 g kg intravenously (IV) over 30 minutes, but its use is controversial because of possible pooling in the area of ischemia and potential worsening of edema. Mannitol can rapidly lower ICP and can be repeated every 6 hours. The maximum dose of mannitol is 2 g...

Diagnosis Clinical Presentation

Paragangliomas can also secrete serotonin and its precursor, 5-hydroxytryptamine. In rare cases, they are associated with the clinical presentation of carcinoid syndrome (bronchoconstriction, abdominal pain, explosive diarrhea, severe headache, cutaneous flushing, hypertension, hepatomegaly, and hyperglycemia).6,15

Basic Mechanisms Of Epileptogenesis

Differences exist between patients who experience a single seizure and those with a tendency for recurrent seizures. Single seizures have various causes including electrolyte disturbances, drugs, and toxins. Increased extracellular K + leading to regenerative hyperexcitability underscores seizures that accompany metabolic aberrations. In hyponatremia, the extracellular space shrinks, leading to an increased concentration of extracellular K + and increased nonsynaptic or ephaptic coupling. This rise in K+ facilitates neuronal firing. Similarly, because membrane excitability varies inversely with the extracellular concentration of Ca 2+ , hypocalcemia can contribute to the synchronization and spread of abnormal electrical activity. Other metabolic disturbances such as hypomagnesemia, hyperglycemia, hypoxia, and ischemia can also produce seizures.


Most of the albumin filtered through the kidneys is reabsorbed, so significant urinary albumin is a sign of abnormal renal function. Large amounts (> 300 mg dL) of albumin can be detected on standard urine dipsticks. Microalbuminuria is defined as a persistent increase of urinary albumin that is below the detectable range of the standard dipstick test. Microalbuminuria is a marker for early diabetic nephropathy and also predicts macrovascular disease. Urinary albumin can be assayed from a spot urine specimen, which is corrected by the urine creatinine, or a 24-hour urine collection. A 24-hour urinary albumin excretion in mg day equates to the same numeric value for the spot urine albumin (mg) creatinine (g) ratio. Therefore the reference ranges for each test are normal < 30, microalbuminuria 30-300, and clinical albuminuria > 300. Factors that may interfere with the test accuracy include strenuous or prolonged exercise, upright posture, hematuria, menses, genital or urinary...


Diabetes mellitus is characterized by hyperglycemia. The American Diabetes Association has defined normal fasting plasma glucose as less than 100 mg dL (5.6 mmol L), prediabetes as 100 to 125 mg dL (5.6-6.9 mmol L), and diabetes mellitus as 126 mg dL (7.0 mmol L) or greater.

Niacin B3

This B-vitamin is also involved in energy-producing reactions in the cells that convert food to energy. In addition, niacin helps maintain healthy skin, nerves, and your digestive system. In some instances, you can use large doses of niacin as a cholesterol-lowering medication. However, you should only do this under the supervision of your doctor. Megadoses can cause hot flashes, itching, ulcers, high blood sugar, and liver damage.

Gestational Diabetes

2-hour postprandial blood sugars below 120 mg dL, insulin therapy is begun. Hemoglobin A1c can be performed every 4 to 6 weeks but will not be elevated unless there is fasting hyper-glycemia. At least weekly evaluation of blood sugar is recommended because insulin resistance increases with advancing gestation. Ultrasonography to assess fetal size should be performed every 4 to 6 weeks. Women requiring insulin should have antenatal testing in the third trimester. Good blood sugar control is also important to decrease the incidence of metabolic newborn complications such as hypoglycemia, hypocal-cemia, polycythemia, and hyperbilirubinemia.

Type D

Type D (Table 10.1) causes enterotoxemia in sheep,4 and is probably most prevalent in young lambs suckling heavily-lactating ewes. It is also the predominant cause of death in weaned animals up to nearly 1 year old, often in those fed rich rations in feedlots. The frequent association of enterotoxemia with upsets in the gut flora caused by an unmanaged change to a rich diet gives rise to the common name of the disease - overeating disease.91 Multiplication of the organism, production of e-toxin,92 and absorption from the gut83 lead to a toxemia with little enteritis. Peritoneal and pericardial effusions are typical.93 e-Toxin's effects on the central nervous system and other tissues result in sudden death, although some animals display dullness, opisthotonos, and convulsions before death.83'91 Hyperglycemia and glycosuria are pathognomonic,83'94 and pulpy kidney, another common name for the disease, derives from the commonly-found post mortem autolysis which rapidly occurs in...

Preterm Labor

Terbutaline has been shown to prolong pregnancy but has not decreased neonatal morbidity.34'39 It is contraindicated in women with pre-existing cardiac arrhythmia. Common adverse effects include hyperglycemia, palpitations, tremor, nausea, headache, and chest pain. Potentially serious maternal adverse effects include pulmonary edema, cardiac arrhythmia, and myocardial ischemia. Reported fetal and neonatal adverse effects include tachycardia, hyperglycemia, and hyperinsulinemia.34

Type 1 Diabetes

The treatment for type 1 diabetes is complex and multifaceted (Wysocki et al. 2003). On a daily basis, children are asked to monitor their dietary intake, monitor and test their blood glucose levels, receive varying amounts of insulin injections, reduce stress, and limit physical overexertion (American Diabetes Association 2009c). Testing of blood glucose levels is usually conducted via finger pricks at set times throughout the day, such as before meals and at bedtime, to inform the child and parent if any changes in dietary intake or insulin administration need to be implemented. Because carbohydrates greatly affect blood sugar levels, children are asked to count or monitor the amount of carbohydrates they consume during meals and snacks. Maintaining a balance of blood glucose is critical for the child's well-being and livelihood. Adhering to this regimen helps to ensure that individuals avoid low or high blood glucose levels (hypoglycemia or hyperglycemia, respectively)....

Common Mechanisms

The pathogenic mechanisms resulting in DM are generally divided into (1) primary defects in beta-cell function, causing variable insulin deficiency (type ldiabetes), and (2) defects in the peripheral action of insulin associated with a slowly evolving loss of the beta cells' ability to compensate (type 2 diabetes). The failure of beta cells in type 1 is most likely caused by autoimmunity, comparable to other disorders affecting endocrine gland function (e.g., Hashimoto's thyroiditis, Addison's disease). Anti-islet cell antibodies are markers of the ongoing process resulting in type 1 diabetes. Beta-cell failure of type 2 diabetes is thought to result from primary genetic defects or acquired dysfunction, as in mitochondrial metabolism that reduces the oxidation of glucose and fatty acids needed for insulin synthesis and secretion. Such defects in mitochondrial function may also account for the peripheral insulin resistance in skeletal muscle, liver, and adipose tissue at the onset of...

Type 2 Diabetes

Older patients with long-term type 2 diabetes with aggressive pharmacologic methods to correct hyperglycemia has failed to improve cardiovascular outcomes (ACCORD, 2008 VADT, 2009). Improved glycemic control in type 2 diabetes, as in type 1, has been shown to preclude progression of small-vessel disease and nerve function disorder to diabetic retinopathy, nephropathy, and neuropathy (UKPDS, 1998a).

Glycemic Targets

Although the efficacy of attaining HbA1c values in the low 7 range resulted in reduced microangiopathic complications, the DCCT and U.K. Prospective Diabetic Study (UKPDS) did not provide conclusive evidence of protection from macrovascular complications. In contrast, UKPDS demonstrated the efficacy of antihypertensive therapy given primarily as a beta blocker or angiotensin-converting enzyme (ACE) inhibitor in slowing the progression of proteinuria and reducing cerebrovascular and cardiac events. Other clinical trials of the statins showed that diabetic patients experience better cardiovascular outcomes with relatively brief treatment. Controlling other major cardiovascular risk factors in DM has a more readily apparent effect on improving diabetic macrovascular outcomes than correction of hyper-glycemia.

Measurement Tools

Blood-sugar control on a day-to-day basis is evaluated by using a glucose monitor. However, it is also recommended that a Hemoglobin A1C (A1C) test be performed at least twice a year in patients who are meeting their blood-sugar goals and every three months in individuals whose blood-sugar levels are not well controlled. The A1C is a simple blood test which shows the average blood glucose level over a three-month period. The following table provides guidelines for blood sugar and A1C goals.

Laboratory Findings

The diagnostic hyperglycemia associated with reduced bicarbonate (HCO3-, usually designated CO2 on a basic metabolic profile BMP ) is accompanied by hyperkalemia in approximately 30 of patients, normokalemia in 50 , and hypokalemia in 15 to 20 . To some extent, serum potassium depends on the severity of the acidosis and duration of the polyuria or vomiting. Hypokalemia is the most dangerous clinical scenario because insulin treatment can cause a precipitous decline in potassium, which may weaken the hyperventilatory effort, causing more profound acidosis and cardiopulmonary arrest. The finding of hypokalemia (and probably even normokalemia) on BMP or electrocardiogram (ECG) with good urine output indicates immediate potassium replacement. In general, hypokalemia on the initial BMP indicates a potassium deficit greater than 400 mEq. Hyperkalemia at the onset of DKA indicates a loss of about 200 mEq of potassium before presentation.


In recent years there has been a growing consensus that the control of high BP in diabetic patients may be more important than the control of hyperglycemia in terms of macroangiopathy. In UKPDS, captopril and atenolol were efficacious in preventing stroke and heart attacks despite less control of blood sugar. These agents were also equal to glycemic control in preventing proteinuria and nephropathy. Given these results, ACE inhibitors have often been recommended as first-line therapy for patients with high BP and diabetes. However, large hypertension trials such as ALLHAT continue to find that diuretics, K-blockers, as well as ACE inhibitors have similar effectiveness in this population and any of these can be used as first-line therapy. Outcomes are also equivalent with ARBs and calcium channel blockers, although these are usually not recommended for initial anti-hypertensive therapy. As noted above, the current recommendation is for lower blood pressure targets in diabetic patients,...

Diabetes Mellitus

Many diabetics and health care providers operate under the misconception that plain sucrose as a sweetener results in hyperglycemia and should be avoided. However, studies have not shown this to be true, and patients do not need to restrict sucrose intake, but rather should monitor the total carbohydrate load in the diet. Some recommend replacing sucrose with fructose in the diet because fructose has a lower glycemic index. There is some concern that fructose adversely affects lipids, however, so this substitution is probably not beneficial. All appear to be safe. Some patients with hyperglycemia need extra protein in the diet 0.8 g protein kg body weight in adults (National Academy of Sciences, 2004). Most adults consume at least 50 more protein than required, so modifying the amount of protein in the diet is usually not necessary for diabetic patients. Dietary intake of the usual amount of protein does not appear to affect the development of nephropathy. However, there are no...


A cataract is a condition that affects a large percentage of the population. As a result, cataract surgery is the most common U.S. surgery performed. Currently, cataracts affect approximately 40 million people in the United States. Generally, the normal aging and cataractous changes in the lens are related to its metabolic activity. Acquired cataracts may be caused by penetrating trauma, irradiation, heat, or blunt trauma. Metabolic cataracts occur particularly in association with diabetes. Changes in the blood glucose concentration may alter the refractive power of the lens. With hyperglycemia, glucose byproducts enter the lens, causing it to swell and inducing a myopic shift. Nuclear sclerosis cataract is the most common cause of lens opacity seen by the ophthalmologist an increased central density makes lens power stronger. As a result, frequent changes in the eyeglass prescription are necessary to correct the changing lens power. This type of cataract develops slowly, and surgery...


Increased mortality was found in both diabetic and stress-induced hyperglycemia groups, independent of age, stroke type and stroke size. Glucose level is an important risk factor for morbidity and mortality after stroke, but it is unclear whether hyperglycemia itself affects stroke outcomes or reflects the severity of the event as a marker. According to the ESO 2008 recommendations (Table 17.2) a blood glucose of 180mg dl (10mmol l) or higher is an indication for treatment with i.v. insulin. According to the American guidelines even lower serum glucose levels, possibly between 140 and 185mg dl, should trigger administration of insulin. In pre-thrombolysis patients, an even more aggressive approach may be advisable. Hyperglycemia

Diabetic Retinopathy

Long-term exposure to elevated blood glucose levels causes damage to pericytes, small cells that surround and support the capillaries of the retinal vascular bed (Resnikoff et al., 2002). Loss of pericytes leads to focal weak spots developing along retinal vascular walls. These weak areas bulge outward, forming microa-neurysms, which leak (causing retinal edema) and eventually burst (causing retinal hemorrhage). This stage of diabetic retinopathy is called background or non-proliferative retinopathy because most diabetics develop at least mild microvascu-lar changes even with relatively good long-term blood glucose control. But the disease does not always stop there. If enough small vessels are affected, retinal tissue distal to these ruptured microaneurysms are deprived of blood and oxygen, and therefore become ischemic. Retinal ischemia promotes retinal angiogenesis, and hence proliferative diabetic retinopathy ensues. This form of the disease is far more visually debilitating...


Patients receiving IV lipid emulsion may be at risk for hyperlipidemia and hyper-triglyceridemia. Hyperglycemia can lead to hypertriglyceridemia and is the most common cause of hypertriglyceridemia in patients receiving PN. Hyperlipidemia in patients receiving PN may lead to a reduction in pulmonary gas diffusion and pulmonary vascular resistance (especially in patients with underlying pulmonary and vascular disease).36 Severe hypertriglyceridemia (especially when serum triglyceride con- to hyperglycemia or impaired lipid clearance or in patients with history of hyperlip- Monitor serum triglyceride concentrations regularly during PN therapy (e.g., at the initiation of PN, then once or twice per week initially, and thereafter depending on clinical condition). If a patient develops hypertriglyceridemia, identify and correct the underlying cause(s) if possible (e.g., treatment of hyperglycemia or reduction of dextrose and or lipid dose). Prolonging the infusion of IV lipid emulsion...

The Diabetic Athlete

Diabetes can be especially challenging as physical activity requires an increased carbohydrate intake. The diabetic must be counseled to check blood sugar levels more often and adjust caloric intake accordingly, because muscle contraction can increase insulin action and glucose uptake. Rapid absorbing carbohydrates in the form of juice or hard candies should be on hand in case of hypoglycemia. As well, the patient's insulin should be readily available. In the event of hyperglycemia (FS > 300), this is best treated by insulin and rest, not exercise.

Oral Agents

The sulfonylureas are the oldest class of drugs and were found to be as safe and effective as insulin in the UKPDS. They shut down membrane potassium ion (K+) channels, allowing membrane calcium (Ca++) channels to open, thereby establishing a calcium gradient that stimulates insulin secretion. In the initial phase of treatment, insulin levels are higher than the previous state following the drug's stimulatory effects. As insulin resistance factors are improved by controlling hyperglycemia, insulin levels fall into a normal range. Treatment is usually effective for 5 to 10 years, depending on the efficacy of behavior treatment and the underlying diabetic progression. The therapeutic duration of sulfonylureas


Hyperglycemia who died from watery diarrhea, hypokalemia, and nephropathy associated with a non-insulin-secreting pancreatic neuroendocrine tumor.43 The diarrhea was so severe that despite intravenous fluids both patients experienced renal failure and death secondary to dehydration. The diarrhea is characteristically large in volume (> 5 L day). It is secretory, which means that it persists despite fasting.44 45 Hypokalemia is present in nearly every patient and is caused by excessive potassium losses in the diarrheal fluid.46-47 The hypokalemia causes severe muscle weakness, which is also a common symptom in these patients, and some are bedridden. Hypochlorhydria is found in 75 of patients with VIPoma and is due to inhibition of gastric acid secretion by VIP.45-48 Flushing, which occurs in a minority of patients, is probably caused by the vasodilatory effects of VIP.45 Hyperglycemia occurs in 25 to 50 of patients and is caused by overcon-version of glycogen to glucose. VIP is a...

Generalized Seizures

Tonic-clonic seizures (TCS) are the most common type of seizure encountered in childhood, adolescence, and adulthood. The manifestations of generalized TCS can be divided into several phases beginning with vague prodromal symptoms that may occur hours to days before the actual convulsion. Common premonitory symptoms include headache, mood change, anxiety, irritability, lethargy, changes in appetite, dizziness, and lightheadedness. The tonic phase may be preceded by a series of brief, bilateral muscle contractions lasting a few seconds. The tonic phase begins with brief flexion of the trunk, accompanied by upward deviation of the eyes, mydriasis, and a characteristic vocalization as contraction of abdominal muscles produces forced expiration across a spasmodic glottis. This process is followed by a period of generalized extension lasting 10 to 15 seconds. With evolution of the clonic phase, tonic contractions alternate with periods of muscle atonia of gradually increasing duration...


Vorinostat inhibits the activity of histone deacetylases which results in repression of gene transcription. Vorinostat is eliminated primarily by glucuronidation and hydrolysis to pharmacologically inactive metabolites, with a terminal half-life of 2 hours. Side effects include diarrhea, fatigue, nausea and anorexia, hypercholesterolemia, hypertriglyceridemia, and hyperglycemia. Despite anemia, thrombocytopenia and neut-ropenia, patients have developed pulmonary embolism and deep vein thromboses while on therapy.

From Ftef

Diabetic Pump Ratio

In the absence of hyperglycemia, these criteria should be confirmed by repeat testing on a different day. The OGTT is not recommended for routine clinical use. DM treatment goals include reducing long-term micro-vascular and macrovascular complications, preventing acute complications from high blood glucose levels, minimizing hypoglycemic episodes, and maintaining the patient's overall quality of life. To achieve these goals, near-normal blood glucose levels are fundamental, thus glycemic control remains the primary objective in diabetes management. Two landmark trials, the Diabetes Control and Complications Trial2 and the United Kingdom Prospective Diabetes Study, showed that lowering blood glucose levels decreased the risk of developing chronic complications. A near-normal blood glucose level can be achieved with appropriate patient education, lifestyle modification, and medications. The only biguanide approved by the FDA and currently available in the United States is metformin....

What Is Fcyiiib

Trans Membrane Signalling Cartioons

In IDDM, the immune system attacks the beta cells in the Islets of Langerhans of the pancreas, destroying them, or damaging them sufficiently to reduce and eventually eliminate insulin production leading to hyperglycemia. The autoimmune attack may be triggered by reaction to an infection.

The Triopathy

Before the landmark DCCT results in 1993, no definitive evidence showed that better control of type 1 diabetes slowed the progression of the common somatic complications of DM neuropathy, retinopathy, and nephropathy. The DCCT showed that in 7 years, the average difference in HbA1c between the conventionally treated diabetic patients and the intensive study cohort of 9.0 versus 7.0 , respectively, resulted in reductions of over 50 for each microangiopathic component of the triopathy. In fact, the investigators discontinued their trial 2 years early to report these remarkable benefits. The UKPDS confirmed the preventive effects of intensive control on reducing diabetic microangiopathic complications in 1998 in patients with type 2 diabetes treated for as long as 15 years. Trials repeatedly reaffirmed that control of hyperglycemia can limit progression of the triopathy in both type 1 and type 2 diabetic patients. How hyperglycemia causes microangiopathy is complex and not fully...

Fastacting Insulins

Elements Earth Wollf

Insulin is a hormone produced in the pancreas and it is responsible for the regulation of glucose uptake and storage. Insulin is most often associated with diabetes mellitus, which is a disease causing hyperglycemia. Healthy people have a basal level of insulin in the bloodstream, but in response to intake of food or to cover glucose clearance from the blood, peaks of larger insulin concentrations appear throughout the 24 h of a day. Patients with diabetes may have difficulties in maintaining the proper insulin concentrations, basal as well as peak concentrations, and accordingly regulation of their insulin level is essential. Type I diabetes patients need insulin to supplement endogenously produced insulin, whereas Type II diabetes patients often are getting insulin in order to improve glycemic control.

Gh somatotropin

Acromegaly Pictures Before After

Hyperglycemia Diagnosis of acromegaly is based on both clinical and biochemical findings. Because secretion of GH fluctuates throughout the day, a single random measurement is never reliable for diagnosing GH excess.1 However, GH-mediated IGF-I production results in relatively stable serum IGF-I concentrations during the day, which correlate positively with 24-hour mean GH levels.1 This makes elevated IGF-I levels an ideal screening test for acromegaly and a reliable monitoring biochemical marker to assess disease activity and response to therapy.6,7 Because IGF-I levels may fluctuate with age and gender, it is important to compare IGF-I levels with age- and sex-matched population values.6,7 Other conditions such as nutritional status, liver dysfunction, insulin levels, and illness also can affect IGF-I levels. The measurement of serum GH secreted by the pituitary in response to an oral glucose tolerance test (OGTT) is the primary biochemical test for diagnosing acromegaly. GH is...


The brain, although not frequently discussed as a target of the complications of chronic diabetes, is nonetheless affected by this disorder. In addition to the neurological complications of glycemic extremes previously discussed (see Hypoglycemia and Hyperglycemia), patients with diabetes have an increased stroke incidence, increased stroke severity, and possibly, a chronic encephalopathy. y Regarding stroke, diabetes increases the risk of large, medium, and small vessel atheroma, as well as arteriolar and capillary microangiopathy, even after other concomitant risk factors (e.g., hypertension) are excluded. 125 In addition, studies have shown that the presence of hyperglycemia at the time of stroke results in more severe brain injury and, hence, a poorer stroke outcome (see Hyperglycemia). CNS abnormalities reported in patients with diabetes include increased P-300 latency, abnormal psychometric tests, and among children with diabetes, lower school achievement test scores.y1...

Cycling PN

14 hours the next day, and then 12 hours the next day). Titrate the PN infusion rate up over 1 to 2 hours to goal rate to avoid hyperglycemia, and taper down over 1 to 2 hours at the end of the cycle to avoid reactive hypoglycemia. Most home infusion pumps can be programmed to cycle a given PN volume automatically over a given time. However, the pharmacist may have to develop an appropriate PN cycle if the infusion pump cannot be programmed. Concerns with cycling PN include hyperglycemia with high infusion rates, reactive hypoglycemia, and fluid and electrolyte abnormalities. Depending on potassium amounts in the daily PN admixture, cyclic PN infusion should also take into consideration the potassium infusion rate that should not exceed 10 mEq h. Reactive hypogly-cemia can be minimized by tapering down PN over 1 to 2 hours before disconnecting. Typically, the nadir will occur around 30 to 60 minutes or even a little over an hour after the PN is stopped. Random capillary blood glucose...

Endocrine System

Postprandial hyperglycemia is common, but because some basal insulin secretion is maintained, fasting hyperglycemia is less severe and ketosis is rare.5 Diet, acute and chronic infection, and corticosteroid use lead to fluctuations in glucose tolerance over time. CFRD is associated with greater nutritional failure, increased pulmonary

Hyperglycemic Crises

Hhs Alogrithm

Metabolic acidosis results from the titration of protons of ketoacids by bicarbonate.37 Once therapy is initiated, a pure hyperchloremic metabolic acidosis may also develop, resulting from extracellular space expansion with sodium chloride (NaCl) and concurrent renal changes. In the hours to days leading up to the marked metabolic changes of DKA, significant water and electrolyte losses occur primarily because of osmotic diuresis. At presentation, total body water, sodium, and potassium are depleted, with deficits in some cases approaching 5 to 8 L, 400 to 700 mEq, and 250 to 700 mEq, respectively. This results in a contracted intravascular space, decreased renal perfusion, a fall in glomerular filtration rate, and reduced renal clearance of both glucose and ketones. Both hyperglycemia and acidosis are thus potentiated. In severe cases, hypotension and vascular collapse may ensue.38 Patients with DKA typically present with hyponatremia because of dilution of the extracellular...


In most cases, hyponatremia is associated with hypo-osmo-lality. Pseudohyponatremia can occur in the presence of other osmotically active substances, such as ethanol, methanol, mannitol, and glucose. Pseudohyponatremia is associated with an osmolar gap, which means the laboratory's measured osmolarity is greater than the calculated osmolar-ity by 10. In the setting of hyperglycemia, every 100-mg dL rise in glucose lowers serum sodium by 1.6 mmol L.

Supportive Measures

Hyperglycemia and hypoglycemia may worsen brain ischemia. When hypoglycemia is present, bolus with 50 dextrose immediately. A blood glucose that is severely elevated should be lowered to less than 200 mg dL (11.1 mmol L) using subcutaneous insulin. Recent guidelines suggest that treatment of hyperglycemia poststroke should be more aggressive than previously recommended. If the patient is febrile, treat with acetaminophen, as fever is associated with brain ischemia and increased morbidity and mortality after stroke. Alternately, cooling devices can be used.7,8 Low-dose un-fractionated heparin (UFH) or low-dose low-molecular-weight heparins (LMWHs) administered subcutaneously will significantly decrease the risk of developing venous thromboembolism (VTE) poststroke. UFH 5,000 units subcutaneously every 8 to 12 hours or low-dose LMWHs should be given for VTE prophylaxis in patients who are not candidates for IV alteplase. In patients receiving IV alteplase, the administration of...

Diabetic Neuropathy

All components of the peripheral nervous system are susceptible, but nerves in the feet are often the first structures to signal the impact of DM. Typically, onset of symptoms occurs in the evening or at night, suggesting nerve dysfunction because capillary peripheral perfusion diminishes with reclining or sleeping. Paresthesias are perceived as numbness, burning, or pins and needles in the toes or the bottom of the foot. Massaging the foot, pushing against a bed board, or walking may help as the microcirculation improves. Remarkably, some patients demonstrate these classic symptoms of diabetic neuropathy even before hyperglycemia occurs in the blood.

Phase I

During phase I, each seizure causes a sharp increase in autonomic activity with elevations in epinephrine, norepinephrine, and steroid plasma concentrations, resulting in hypertension, tachycardia, hyperglycemia, hyperthermia, sweating, and salivation. Cerebral blood flow is also increased to preserve the oxygen supply to the brain during this period of high metabolic demand. Increases in sympathetic and parasympathetic stimulation with muscle hypoxia can lead to ventricular arrhythmias, severe acidosis, and rhabdomyolysis, which could then lead to hypotension, shock, hyperkalemia, and acute tubular necrosis.

Initiating PN

Exercise caution when initiating PN to avoid hyperglycemia, and fluid and electrolyte abnormalities. Once the goal daily volume is determined, infuse the PN admixture first over 24 hours. For safety, initiate PN at a lower infusion rate (e.g., approximately 50 of goal for anywhere from approximately 12 to 24 hours) on day 1 with no more than 150 to 200 g of dextrose per day (or a maximum dextrose infusion rate of approximately 2 mg kg min). Then increase PN up to goal over the following approximately 12

Indications for PN

PN can be a lifesaving therapy in patients with intestinal failure, but the oral or enteral route is preferred when providing nutrition support therapy (when the gut works, use it). Compared with PN, enteral nutrition is associated with lower risk of hyperglycemia and fewer infectious complications (e.g., pneumonia, intra-abdominal abs-

Insulin Rebound

A diabetic complication that family physicians routinely manage is caused by nighttime or very-early-morning hypo-glycemia, which leads to fasting hyperglycemia and sometimes ketosis, especially in children (Somogyi effect). If the patient and physician are not careful, they can get caught in a spiral of ever-increasing insulin doses in response to rebounding glucose values. When confronting persisting morning hyperglycemia, the first step is for the patient to monitor 3 am glucose levels. If low, reduced dosage or timing change in evening insulin administration is necessary.

Basal Bolus Insulin

The starting dosage of insulin as previously discussed is often a conservative approximation. In general, a type 1 diabetic patient requires approximately 0.5 U kg, half of which is given as basal insulin and the other half in divided boluses before a meal. Experience and clinical judgment may suggest a lower starting dosage if the diabetes is mild, especially with children and elderly patients, who may receive a starting dose of 0.1 or 0.2 U kg day. However, hyperglycemia may have resulted in secondary insulin resistance caused by cellular dysfunction, and higher dosages may quickly become necessary. If the patient is not at risk of ketoacidosis, cautiously increasing the dosage from 0.5 U kg day is prudent (usually by 10 per day). The effectiveness of a specific dose of most insulin preparations depends on local factors at the injection site related to capillary perfusion. Insulin uptake is enhanced when hydration is adequate and a patient is vasodilated after exercise or a warm...

Risk factor diabetes

Toothfairy Letter

There are two main types of diabetes. Type 1 diabetes, in which the pancreas stops making insulin, accounts for 10 to 15 of cases. The majority of people with diabetes have type 2 disease, in which insulin is produced in smaller amounts than needed, or is not properly effective. This form is preventable, because it is related to physical inactivity, excess calorie intake and obesity. People with type 1 diabetes need insulin injections to lower blood sugar, but many people with type 2 do not.

Subject Index

Hydatid cysts, 110 hydatidosis, 110 hydrocele, 126 hydrocephalus, 100 hydronephrosis, 291 hydrophobia (rabies), 115, 270-75 hydrothorax, 100, 102-4 hydroureter, 291 Hymenolepsis nana, 319-20 hypercholesterolemia, 101 hyperesthesia, 359 hyperglycemia, 92 hyperkeratosis, 251 hyperlipidemia, 155 hyperpiesis. See hypertension hyperplasia, 68, 182 hypertension, 169-71 characteristics, 169-70 dropsy and, 101 eclampsia and, 110-12 gangrene and, 138 gout and, 155 history, 170-71 primary vs. secondary, 169 salt-sensitive, 170 strokes and, 33 WHO classification, 169 hyperthyroidism, 237 hyperuricemia, 153-56 hyperventilation tetany, 328 hypocalcemia, 328 hypocalcemic convulsions, 329-30 hypochromic anemia, 73 hypoglycemia, 219, 263-64 hypomagnesemic convulsions, 329-30


Occasionally, a diabetic mononeuritis with a localized region of pain can be misdiagnosed clinically as a mechanically mediated neuritis, such as a herniated intravertebral disk. If the appropriate imaging studies fail to demonstrate a mechanical etiology, a presumptive diagnosis of diabetes neuritis should be made and treatment aimed at glycemic control with physical therapy. On the other hand, diabetic neuritis of this type with constant pain may be initiated by mechanical factors. For example, a diabetic patient may acutely injure spinal nerves with a lifting maneuver, but this neuromuscular pain may become a continuing neuropathic pain as diabetic nerve fibers fail to heal in the presence of marked hyperglycemia. With no other etiologies evident, these patients eventually improve with more effective diabetic management.