Home Cure for Hypoglycemia

Guide To Beating Hypoglycemia

Here's Just A Tiny Glimpse Of The Topics Covered: The 3 main types of hypoglycemia and which type you're most likely suffering from. How snacking on chocolate bars can actually make you Fat and worsen your condition! (If you thought those delicious dark brown bars were great energy- boosters.think again!) The No. 1 question most folks have when it comes to hypoglycemia and hyperglycemia. Why you should insist on a 6-hour Gtt and not a 5-hour one. ( Why it might not be a good idea to consult a doctor to confirm your hypoglycemia. Aside from taking a Gtt, what other methods can you use to determine whether or not you're suffering from this condition? Well, refer Chapter 4, Pgs. 23-26 to take a revealing 67-question test especially designed to find out if you've got the symptoms. An inspiring motivational exercise that will help you effectively banish all of your negative thoughts that prevent you from having peace of mind. 2 good reasons why you should keep a food journal. 3 powerful nutrients that limit the effect of glucose on your blood sugar level. This is vital to a hypoglycemic as it helps slow down the absorption of sugar in the food. The secret impulse that literally forces you to say 'yes' to a candy bar or chocolate whenever you feel the hunger pangs gnawing at you. 2 ingredients that are lethal to a hypoglycemic. 'Hidden sugars' you must know to avoid buying products that can easily worsen your condition. 8 essential rules of food planning that are crucial to your speedy recovery from hypoglycemia. Leave out one of them and it could hurt your chances of recovering. How to create a healthy food plan that's suitable for both vegetarian and non- vegetarian hypoglycemics. Most food plans only focus on non-vegetarians, but this one works great for everybody!

Guide To Beating Hypoglycemia Summary

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Endocrine Pancreas and Hypoglycemia

An important physiologic role of the endocrine pancreas is protecting the body against hypoglycemia, which is undertaken by the release of glucagon to counteract the fall in glucose. A large number of studies have been directed at establishing the mechanisms underlying the glucagon response to hypoglycemia, and it has been demonstrated that it is caused by an increase in both parasympathetic and sympathetic neural activity and by elevated levels of epinephrine secreted by the adrenal medulla.162 The importance of the neural effects for this response has been demonstrated in humans, in whom infusion of a ganglionic blocker has been found to inhibit the glucagon response to hypoglycemia.163 A similar response is that seen during neuroglycopenia, when a local reduction of glucose in the brain cells initiates activation of the autonomic nervous system to increase the secretion of glucagon and, in some species, also insulin.64164 Neuroglycopenia is induced experimentally by an intravenous...

Glucose Metabolism Disorders Hypoglycemia

Unlike other body tissues, the CNS relies almost exclusively on glucose as an energy substrate. CNS features that promote its vulnerability to hypoglycemia include its low glucose level (about 25 percent of the serum glucose value), its inability to store significant glucose as glycogen, and the high cerebral metabolic rate (5 mg 100 g brain tissue min) for glucose. yj Thus, for a 1400 g brain, the glucose requirement is 70 mg min. The brain's dependence on glucose, coupled with its limited glycogen stores, results in rapid CNS dysfunction when hypoglycemia occurs and permanent neurological sequelae if it is prolonged. The glucose level at which CNS dysfunction occurs depends on its rapidity of onset, the current level of CNS activity, the quantity of CNS glycogen, and the availability of alternative fuels. The immediate cause of CNS dysfunction is unknown. Although it was initially believed to be due to tissue energy depletion, high-energy organic...

Differential Diagnosis of Hypoglycemia

Sulfonylureas And Hypoglycemia Visits

As shown in Table 79-2, there are many causes of hypoglycemia. Hypoglycemia may be due to inhibition of glucose production in the liver and stimulation of glucose utilization by adipose and muscle cells. Hypoglycemic attacks secondary to an insulinoma are predominantly due to an overuse of glucose by the cells in the body. These attacks are episodic because of the intermittent secretion of insulin, especially in Postprandial (reactive hypoglycemia) Fasting hypoglycemia Glyucos e-6-phosphatas e Liver phosphorylase Pyruvate carboxylase Phosphoenoipyruvate carboxykinase Fructose 1,6-biphosphate Glycogen synthetase Substrate deficiency Ketotic hypoglycemia of infancy Severe malnutrition, muscie wasting Late pregnancy Acquired liver disease Hepatic congestion Severe hepatitis Cirrhosis Drugs Alcohol Propranolol Salicylates early cases. It is not until advanced or metastatic disease is present that persistent hypoglycemia may ensue. This state of excessive glucose utilization should be...

Hypoglycemia

Hypoglycemia is relatively common in the newborn infant. In the healthy term newborn, low blood glucose concentrations are often encountered and usually reflect normal metabolic adaptation to extrauterine life. However, with prolonged or recurrent hypoglycemia, the newborn risks neurologic sequelae (Fluge, 1975). The blood glucose level that defines clinically significant hypoglycemia is controversial. Cornblath and associates (2000) believe that a plasma glucose concentration less than 36 mg dL warrants close monitoring. If the plasma Infants who are known to be at higher risk for hypogly-cemia should have blood glucose concentrations routinely measured. Infants at high risk for hypoglycemia include infants of diabetic mothers (IDMs), small-for-gestational-age (SGA) newborns, infants with a history of perinatal hypoxia or ischemia, and infants who become hypothermic from cold stress. Infants who become septic are also at higher risk for hypoglycemia. For infants at risk, glucose...

Hypoglycemic Crises

Hypoglycemia, defined as a blood glucose level less than 50 mg dL, occurs in a wide variety of clinical settings.45 This results from a failure of the normal homeostatic mechanisms previously discussed to achieve a balance in glucose production and utilization. In normal subjects, as plasma glucose decreases below the physiologic range, the counter-regulatory hormones epinephrine and glucagon are released followed by growth hormone and, ultimately, Cortisol. Signs and symptoms of hypoglycemia are categorized as adrenergic and neurogly-copenic in origin.46 The glycemic threshold for epinephrine release is higher than that for neuroglycopenic symptoms and is reproducible for a given individual, although there is considerable variability between subjects.47 The physical sequelae of epinephrine release in response to hypoglycemia include pallor, diaphoresis, tachycardia, nausea, and anxiety. Because glucose is the preferred energy source for the central nervous system, neuroglycopenic...

Anxiety and Obsessive Compulsive Disorder Syndromes

Anxiety is an extremely common occurrence that affects everyone at some time and is characterized by an unpleasant and unjustified sense of fear that is usually associated with autonomic symptoms including hypervigilance, palpitations, sweating, lightheadedness, hyperventilation, diarrhea, and urinary frequency as well as fatigue and insomnia. Anxiety is thought to be mediated through the limbic system, particularly the cingulate gyrus and the septal-hippocampal pathway, as well as the frontal and temporal cortex. The term anxiety disorder is used to denote significant distress and dysfunction resulting from anxiety, including panic attacks and anxiety with specific phobias. Chronic, moderately severe anxiety tends to run in families and may be associated with other anxiety disorders or depression. The differential diagnosis of anxiety states includes other psychiatric conditions such as anxious depression as well as schizophrenia, which may present as a panic attack with disordered...

Effect of training on the hormonal response to exercise

Other stressful stimuli, e.g. hypoxia or hypoglycemia is in fact increased in the trained state and it is well known that the secretory capacity of the adrenal medulla is increased by endurance training 'sports adrenal medulla' 62 . Trained individuals display lower insulin concentrations in plasma, during both basal and glucose-stimulated conditions, secondary to a decreased pancreatic insulin secretory rate 32 and an increased peripheral insulin sensitivity 69 . Training augments the lipolytic capacity of the adipocyte, which serves to maintain a sufficient lipolytic rate in a trained individual, in spite of a reduced sympathetic activation during exercise at a given intensity 70 . Endurance training also increases the oxidative capacity of the liver as well as the hepatic capacity for gluconeo-genesis, although the glucose demand during exercise is clearly decreased in the trained state, as discussed above. This decreased demand is sensed by the body and as little as 10 days of...

Theoretical Framework For Understanding Stress Responsive Systems

Perhaps the most important distinction between environmental and physiological stressors is that physiological stressors do not necessarily require cognitive appraisal, emotional evaluation, or conscious awareness to exert their effects. For instance, exposure to infectious agents (bacteria, viruses, toxins, etc.), hypoxia, hypoglycemia, and hypothermia are all examples of physiological stressors that elicit a stress reaction. Clearly, once the seriousness of the physiological challenge passes some identifiable threshold, the individual would normally develop a subjective experience of stress, which may then further activate stress responsive systems. Nevertheless, psychic stressors are qualitatively different than environmental ones and may activate stress responses via distinct pathways (Herman et al., 1996 Herman and Cullinan, 1997).

Sympathetic Nervous System

On the other end of the spectrum would be physiological threats to homeostasis such as hypoxia, hypoglycemia, or hemorrhagic shock that are detected in brainstem structures such as the pons, medulla, and reticular formation. In cases such as these where threat is not necessarily detected by the cognitive or perceptual apparatus of the organism, but rather by alarm systems that continuously monitor peripheral physiological status, the locus coeruleus sends ascending catecholaminergic input to higher brain centers. Such information is then processed by higher cognitive structures in order to encourage behavioral strategies that will alleviate the threat to homeostasis. Thus, brainstem autonomic nuclei such as the locus coeruleus are critical sites of integration for threatening stimuli irrespective of whether the threat originates from higher brain centers or peripheral challenges to homeostasis see Harro and Oreland (2001) for an excellent review .

Etiology And Epidemiology

Oral contraceptives, hormone therapy, oral hypoglycemic agents, anticonvulsants, and opioids are other common therapies that can cause nausea and vomiting.1,6 Some medications, such as digoxin and theophylline, cause nausea and vomiting in a dose-related fashion. Nausea and vomiting may indicate higher-than-desired drug concentrations. Ethanol and other toxins also cause nausea and vomiting. Oil hypoglycemics

General Medical Therapy

Seizures are prevalent in patients with glioma, particularly in slowly growing, low-grade gliomas, and require adequate management. Clinicians should recognize the possibility that seizures could be caused by hyponatremia, hypoglycemia, and hypocalcemia, as well as by mass effect. Seizures are generally managed with standard anticonvulsants, including phenytoin, phenobarbital, primidone, gabapentin, lamotrigine, carba-mazepine, valproic acid, and clonazepam. Anticonvulsants, which are generally dose dependent, can interact with drugs that are commonly given to patients with brain tumors to produce adverse effects, some of which are drowsiness, dizziness, ataxia, nausea, vomiting, confusion, constipation, tremor, hypersalivation, and blurred vision.

Infant of a Diabetic Mother

The incidence of hypoglycemia in the IDM ranges from 25 to 40 . Many nurseries have protocols for the IDM that include checking a bedside whole-blood glucose measurement at 30 minutes of age and again at 1 and 2 hours of age. If the whole blood cell glucose value is reported as less than 40 mg dL, a serum glucose should be obtained and the

Epidemiology and Clinical Phenotype

Although the tumors most commonly described in MEN1 are not malignant, they are often associated with medical conditions that require therapeutic intervention. Symptoms in this disorder are therefore related to the biology of the tumors occurring in any one affected individual. Symptoms are most often related to hypersecretion of various hormones secondary to these tumors. Glucose intolerance, hypoglycemia, hypergastrinemia with severe peptic ulcer dis-

Medium Chain AcylCoA Dehydrogenase Deficiency

Most patients present between ages 3 and 15 months, rarely after 4 years. Phenotypical heterogeneity prevails, ranging from sudden infant death syndrome, to recurrent Reye's-like syndrome, to episodic nonketotic hypoglycemic coma. A common presentation is vomiting and lethargy, followed by fasting, associated with a prior viral respiratory or gastrointestinal infection. Presentation is usually to an emergency department as an acute toxic encephalopathy or coma, with hypoketotic hypoglycemia, hyperammonemia, and abnormal liver function tests. Ihe serum carnitine value is low, and urine acylcarnitines are increased, with a specific profile. Enzyme assay for MCAD activity can be done on cultured skin fibroblasts, muscle, liver, or blood lymphocytes. Ihe differential diagnosis includes other fatty acid oxidation disorders, exogenous toxic encephalopathies, and true Reye's syndrome. Specific management involves intravenous dextrose 10 percent, avoidance of fasting with frequent short...

How Do Hormones And Epilepsy Interact

Hormones affect seizures, and seizures affect hormonal regulation and secretion. Thyrotoxicosis, hyponatremia associated with the syndrome of inappropriate antidiuretic hormone secretion (SIADH), and hypoglycemia all lower seizure thresholds in epileptic patients and may trigger de novo situational seizures. These facts are noted in the standard medical textbooks and do not need to be discussed here. However, more subtle manifestations of hormonal influences on seizures and vice versa may easily be overlooked because they are not usually emphasized in the training of neurologists. Awareness of how different hormones relieve or exacerbate seizures may lead to improvement in the treatment of seizures with the use of adjunctive hormonal therapy. Seizure effects on hormonal physiology, for instance reproductive and sexual functioning, may result in significant impairment of the patient's life in addition to the effect of the seizures themselves for instance infertility or impotence....

Clinical Manifestations and Pathology

Upon examination, the liver and spleen frequently are found to be enlarged, and a range of other symptoms have been documented. Among the more common are anemia and vitamin A deficiency, with some vision impairment, a range of micro-nutrient deficiencies, plus tendencies to hypothermia, higher bilirubin, hyponatremia, hypoglycemia, and very low plasma albumin. The overt symptoms of classical marasmus are far fewer and less medically unusual. There is extreme wasting of both muscles and subcutaneous tissues, and stunting is quite marked. Because the victim is so emaciated, the head appears abnormally large, especially the eyes. The skin tends to be dry and patchy, but dermatosis is not seen, nor are there any significant hair changes. Anorexia is uncommon, and, in fact, the appetite is usually good, which helps to simplify therapy. As in kwashiorkor, there is likely to be hypothermia and a tendency to hypoglycemia. Dehydration is a problem as marasmus worsens, and behavior changes from...

Pancreas Transplantation

Whole-organ pancreas transplantation is a major surgical procedure with a significant rate of morbidity and the need for immunosuppression. However, it improves the patient's quality of life and reverses some diabetic complications, and up to 82 insulin independence at 1 year is reported.82 Pancreas transplantation can be performed simultaneously with kidney transplantation (SPK), as occurs in approximately 90 of patients, or after kidney transplantation (4 ) and in specialized enters in nonuremic patients as pancreas transplantation alone (6 ).82 Survival rates are better for SPK because acute rejection can be treated earlier, coinciding with the simultaneous rise in serum creatinine that is indicative of acute rejection of the kidney. Pancreas transplantation in a nonuremic patient is performed more rarely. These patients have brittle (labile) diabetes or hypoglycemic unaware-ness that is regarded as potentially more harmful than the combined risk of the immunosuppression and...

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...

Cell Biology of Islet B Cells

When glucose has entered the B cells, it is phosphorylated by glucokinase to glucose 6-phosphate.115 The glycolytic activity in the glucose-exposed islet is basically regulated by glucokinase acting as the rate-limiting enzyme in the flux of substrates through the glycolysis. The glucokinase activity has therefore been recognized as the B-cell glucose sensor.116 After its phosphorylation, glucose is metabolized and adenosine triphosphate (ATP) is formed.117 An increased intracellular content of ATP or rather an increased ratio of ATP to ADP (adenosine diphosphate) leads to closure of specific ATP-regulated potassium (K+) channels in the plasma membrane.118 This leads to a decreased outflow of K+ from the B cells, which, in turn, depolarizes the cells, resulting in the opening of L-type voltage-sensitive Ca2+ channels.119 This causes a massive inflow of Ca2+ from the extracellular space because the cytoplasmic free concentration of Ca2+ under resting conditions is only approximately...

Cell Biology of Islet NonB Cells

The mechanisms by which nutrients stimulate insulin secretion, including the signal transduction pathways of the B cells, have been extensively studied. Much less is known about the other islet cell types, including the mechanisms behind modulation of glucagon secretion. Glucagon is secreted from A cells in response to low blood glucose, and thus the secretion is decreased as glucose increases. It has been shown that pyruvate metabolism in the mitochondria is implicated in the initiation of glucagon secretion141 and that the mechanism of action seems to involve closure of ATP-regulated K+ channels, which have been shown to be expressed on islet A cells together with voltage-dependent Ca2+ channels.142,143 Furthermore, as in most exocytotic events, Ca2+ and ATP are required in glucagon secretion. In B cells, glucose increases ATP production and elevates intracellular Ca2+ however, in A cells, ATP production is much less increased and Ca2+ is barely changed after glucose stimulation.141...

Endocrine Pancreas and Stress

Hepatic glucose delivery drops, leading to hypoglycemia. Hence, the endocrine pancreas ensures an optimal discharge of insulin until the septic insult becomes too strong. The mechanism of the hypersecretion of insulin during sepsis remains to be established. In one study, it was demonstrated that the glucose-induced insulin secretion from isolated islet cells was the same in septic rats as in control rats, indicating first, that islet cells derived from septic animals have a preserved insulin secretory capacity and second, that the hypersecretion observed in vivo is probably mediated by an indirect mechanism, hypothetically by neural influences or inflammatory mediators.175

Historical Background

Tumors of pancreatic islet cell origin were described by Nicholls1 as early as 1902, well before the discovery of insulin by Banting and Best in 1922.2 It was known that some islet tumor extracts produced hypoglycemia when introduced into dogs however, not until insulin was discovered was the significance of this observation appreciated. Harris3 described the clinical pathophysiology of hyperinsulinemia in 1924 but did not associate the presentation of symptoms with islet cell adenomas of the pancreas. Shortly thereafter, Wilder and colleagues reported the first exploration for this tumor by William J. Mayo in 1926.4 Unfortunately, the patient, a physician with an 18-month history of severe hypoglycemic attacks, was found to have a large, unresectable malignant insulinoma with hepatic metastases. The patient died within 1 month of surgery. An autopsy also revealed the presence of renal calculi, suggesting that this patient had multiple endocrine neoplasia type 1 (MEN 1). Roscoe Graham...

Sporadic Endocrine Pancreatic Tumors

In approximately 5 of insulinomas, the only manifestation of malignancy is local infiltration. These tumors are usually curable by resection if no hepatic metastases are present. When resection is indicated on the basis of location or size, we attempt splenic preservation whenever possible. This is usually feasible unless the splenic vein is within the posterior pancreatic parenchyma. If malignancy is suspected, a distal resection in continuity with the spleen and peripancreatic lymph nodes is performed. For patients with hypoglycemia caused by islet cell hyperplasia or nesidioblastosis rather than a tumor, a distal pancreatectomy to the level of the superior mesenteric vein is performed in those whose hypoglycemia is responsive to a trial of preoperative diazoxide testing. A more extensive (85 ) resection is done in those patients who are refractory to this drug in preoperative testing.5 We currently use only endoscopic ultrasonography (EUS) for preoperative localization when...

Family Education Programs

One such program focused on families with children with insulin-dependent diabetes mellitus (Laf-fel et al. 2003). This program included standardized teaching about the illness that focused on methods of family illness problem solving, including responses to elevated or low blood sugar, and assisted family members in keeping diabetes-related records. Among the children in the study group, diabetes control was improved and medical complications reduced. Other similarly designed and structured education programs have shown an increase in illness knowledge and enhanced illness management behavior among families (Boschen et al. 2007). However, one meta-analysis of 11 self-management teaching programs for pediatric asthma (Bernard-Bonnin et al. 1995) found no reduction in school absenteeism, frequency of asthma attacks, hospital-izations, or emergency department visits, and the authors concluded that future programs should focus more on intermediate outcomes such as behavior. Nonetheless,...

Non Multiple Endocrine Neoplasia Endocrine Syndromes

Beckwith-Wiedemann syndrome is a disorder usually recognized at birth and characterized by a variable constellation of findings, including hemihypertrophy, macroglossia, gigantism, malrotation, and visceromegaly.8 Islet cell hyperplasia with associated hypoglycemia, Wilms' tumor, adrenocortical abnormalities including carcinoma with associated Cushing's syndrome, gonadal hyperplasia, and liver abnormalities ranging from focal nodular hyperplasia to hepatoblastoma have also been described. Mental retardation has been noted in several patients with this disorder as well, although it is not clear whether it is related to the hypoglycemia associated with the nesidioblastosis and seen in more than half of these patients. Beckwith first described these patients in 1963 and pondered whether this was a discrete syndrome.9 Wiedemann reported on additional families shortly after and also suggested a new syndrome.10 Irving labeled this disorder the EMG syndrome, for exomphalos, macroglossia, and...

Hormonal Regulation of Glucose Metabolism

Glucagon was identified in 1923 as the hyperglycemic component of canine pancreatic extracts.20 The glucagon gene is located on the long arm of chromosome 221 and is expressed in pancreatic alpha cells, small intestinal L cells, and certain hypothalamic cells.22 Tissue-specific enzymes permit cell-selective cleavage of preproglucagon into various peptides such as glicentin (enteroglucagon), oxyntomodulin, and GLP, but only alpha cells produce glucagon.23 Glucagon is the primary guarantor of cerebral fuel delivery and is regulated by both glucose and insulin.24 In the human islet the different endocrine cell types are arranged in a nonrandom fashion, with the glucagon-producing alpha cells surrounding a beta-cell core.25 Glucose acts directly on alpha cells to suppress glucagon release. In addition, insulin secreted into the islet microcirculation from centrally located beta cells potently inhibits glucagon secretion.26 Glucagon secretion is also influenced by adrenergic, cholinergic,...

Pharmacologic therapy

The IV quinidine regimen requires close monitoring of the ECG (QT-seg-ment) and other vital signs (hypotension and hypoglycemia). An alternative oral treatment for P. falciparum infections in adults, especially those with history of seizures, psychiatric disorders, or cardiovascular problems, is the combination of atovaquone 250 mg and proguanil 100 mg (Malarone) (two tablets twice daily for 3 days).1 The pediatric dose of Malarone is as follows child less than 5 kg not indicated 9 to 10 kg 3 pediatric tablets day x 3 days 11 to 20 kg one adult tablet day x 3 days 21 to 30 kg 2 adult tablets day 3 days 31 to 40 kg 3 adult tablets day 3 days greater than 40 kg 2 adults tablets twice daily x 3 days. Since falciparum malaria is associated with serious complications, including pulmonary edema, hypoglycemia, jaundice, renal failure, confusion, delirium, seizures, coma, and death careful monitoring of fluid status and hemodynamic parameters is mandatory. Exchange transfusion...

Migraine with Aura Classic Migraine

Migraine-like headaches with or without aura may occur as a result of a wide variety of structural abnormalities of the brain, including tumors, infections, and vascular malformations. Such headaches may be thought of as secondary migraine. Cerebrovascular disorders such as infarction, transient ischemic attack, venous thrombosis, vasculitis, and carotid or vertebral dissection should be included in the differentiation of migraine. Idiopathic intracranial hypertension (IIH), low pressure headache, and intracranial neoplasms may also mimic migraine, as may metabolic abnormalities, hypoxia, hypoglycemia, dialysis, pheochromocytoma, and various chemicals and medications. Raeder's syndrome, with carotid artery abnormalities along the base of the skull, may also resemble migraine. Sinusitis or glaucoma may occasionally resemble migraine, and sometimes epilepsy produces intermittent headaches. Although rare, the aura of migraine may lead directly to a partial or...

Autonomic Dysfunction Secondary to Focal Central Nervous System Disease

Hyperhidrosis may be generalized or localized. Localized hyperhidrosis is rare and may occur with injury to the spinal cord (e.g., in syringomyelia), peripheral nerves (e.g., with partial median or sciatic nerve injury), or eccrine sweat glands. Perilesional hyperhidrosis may surround an anhidrotic region produced by a lesion of the sympathetic ganglia or rami. The axillary eccrine sweat glands are activated by thermal stimuli, whereas the palmar and plantar glands are activated by emotional stimuli. Primary or essential hyperhidrosis affects the axillary, palmar, and plantar regions and may be familial. Generalized hyperhidrosis may be secondary to infections, malignancies, or neuroendocrine disorders (e.g., pheochromocytoma, thyrotoxicosis, acromegaly, carcinoid, anxiety, hypotension, hypoglycemia, and cholinergic agents).y

Carbohydrate Metabolism

The normalization of biochemical abnormalities, especially that of calcium, has a much greater impact on insulin sensitivity than on insulin secretion.100 Postoperative correction of the hypercalcemic state leads to an increased insulin sensitivity and, therefore, to the possibility of severe hypoglycemia in insulin-dependant diabetes.15118 Improved metabolic control was achieved in 27 of patients with PHPT after parathyroidectomy.15 Prager and associates102 also showed partial improvement in glucose utilization after parathyroidectomy. These patients were clinically symptomatic, and this might explain the more pronounced disturbance of carbohydrate metabolism.

Degenerative Unverricht Lundborg

Hypoglycemia Hypoglycemia 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,...

Herb Drug Interactions

Supplements that May Raise Blood Glucose Includes the most frequently used herbs list is not comprehensive. Derived from expert opinion, case reports, preliminary trial evidence, and anecdote. Note that these effects can potentially have therapeutic benefit in diabetic or hypoglycemic patients.

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. Basal insulin can be given to fasting patients at starting dosages of 0.25 U...

Cranial Nerve Dysfunction

The plasma glucose exceeds 500 mg dl. The reason for this decrease is unclear, but it may reflect the saturation of the carrier-mediated transport of glucose at high plasma concentrations. As a result, it is important to obtain a concomitant serum glucose level at the time of the CSF sample. Although an elevated CSF glucose level (hyperglycorrachia) results from an elevated plasma glucose level, a decreased CSF glucose concentration (hypoglycorrachia) may be due to a variety of causes including hypoglycemia. The other etiologies include bacterial meningitis y (including typical bacteria, tuberculosis, and neurosyphilis), fungal meningitis, certain viral meningitides (mumps),y subarachnoid hemorrhage, carcinomatosis meningitis, chemical meningitis, and meningitis resulting from parasitic organisms (cysticercosis, trichinosis, amebiasis). If 0.4 is used as the lower limit of the normal CSF to serum glucose ratio, values below 0.4 have a sensitivity of 80 to 91 percent and a specificity...

PAdrenergic Antagonists

Ocular medication requires the use of concentrated drug solutions to penetrate the eye. Excess drug drains into the nose via the nasolacrimal duct where it is absorbed into the systemic circulation. B-Blockers can cause significant systemic adverse effects through this pathway, because first-pass hepatic metabolism is bypassed resulting in pharmacologically significant serum drug concentrations.36 Bronchospasm is the most common pulmonary effect of topical B-blockers. Pulmonary edema, status asthmaticus, and respiratory arrest have been reported with B-blockers as well. Cardiovascular effects include bradycardia, hypotension, and congestive heart failure exacerbation. As with systemic B-blockers, topical B-blockers have also been reported to cause depression, hyperlipidemia, and mask symptoms of hypoglycemia. Topical ft-blockers are generally contraindicated in patients with asthma, chronic obstructive pulmonary disease (COPD), sinus bradycardia, second or third degree heart block,...

What Complications Can Occur With Convulsive Status Epilepticus

Blood flow and cerebral metabolism are elevated in early SE but decline eventually, and the excessive metabolism of discharging neurons may outstrip the oxygen and glucose supply.12 As seizures continue, autoregulation may break down and contribute to cerebral edema, particularly in children. Many physiologic changes of early SE appear to reverse after about 30 min, with subsequent hypotension, hypoxemia, hypoglycemia, and increasing acidosis and hyperkalemia. There Fever, sweating, hypersecretion (including tracheobronchial), vomiting Hyperkalemia, hyperglycemia then hypoglycemia, volume depletion, venous

Factors affecting serum testosterone levels in elderly men

Both physical and psychological stress and strenuous physical activity have been shown to result in depressed testosterone levels (Nilsson etal. 1995 Opstad 1992 Theorell et al. 1990). Acute fasting may transiently affect testosterone production through diminished gonadotropic testicular drive (Cameron et al. 1991), although elderly men may be more resistant to the metabolic stress of fasting (Bergendahl et al. 1998). Similarly, serum testosterone levels in elderly men were found to be less affected than those in young men during induced hypoglycemia and in the acute phase following myocardial infarction (Deslypere and Vermeulen 1984).

Drug Delivery by Chimeric Peptides

Quantitative measurements of the uptake of cationized proteins as vectors in chimeric peptides were subsequently performed with cationized human albumin conjugated to avidin. Vectors utilizing receptor-mediated uptake must avoid competition by endogenous ligands, as discussed for transferrin above, and also should not display undesirable intrinsic pharmacological activity. Therefore, the use of insulin, with its effect as a hypoglycemic hormone, would be undesirable. Despite these caveats, experimental evidence in favor of the potential utility of insulin peptides in a delivery system has been presented with an insulin fragment one tryptic fragment with low receptor binding affinity (10 of the affinity of insulin) was devoid of a hypoglycemic effect in mice in vivo, yet a chimeric peptide synthesized with horseradish peroxidase was transported into brain in vivo and reached a brain concentration of 1.41 of the injected dose after intravenous administration to mice (105).

Pathomechanism and hormonal dysregulation in overtraining

Sults represent an interesting parallel to the reduced response of ACTH, growth hormone and cortisol to an insulin-induced hypoglycemia in four overtrained marathon runners, in whom the pituitary response to luteinizing hormone (LH) was unaffected 62 . It was concluded that a hypothalamic dysfunction exists in OTS. These impaired hormonal reactions of overtrained athletes contrast with the usually increased levels induced by training.

Table 305 Glycogenoses

Clinical Features and Associated Disorders. In Von Gierke's disease, hypoglycemia causes many of the clinical difficulties seen in patients during the first year of life. In this period seizures are frequent, and long-standing hemiplegia and mental retardation occur. Failure to thrive, xanthomas, and isolated hepatomegaly are common, and excessive subcutaneous fat over the buttocks, breasts, and cheeks develops. Affected children usually have a protruding abdomen due to enlargement of the liver. Patients often have recurrent stomatitis frequent infections and may have isolated chronic inflammatory bowel disease. been identified infantile, childhood, and adult. In the infantile type, early symptoms are similar to, but less marked than, those typical of Von Gierke's disease, which is associated with hypoglycemia, failure to thrive, and hepatomegaly. Patients with the infantile type are hypotonic and weak and have poor head control. Juvenile-onset debrancher enzyme deficiency begins...

Perioperative Management of Serum Glucose

Until the tumor is removed, the mainstay of therapy is the prevention of hypoglycemia. This may entail frequent meals and minimizing prolonged exercise. Intravenous glucose should be given the night before surgery, especially after the patient ceases oral intake. Administration of diazoxide or the somatostatin analog octreotide is employed preoperatively in some c nters, not only to control hypoglycemic attacks but also to determine the patient's response and tolerance to such therapy should surgical exploration be unsuccessful. We rarely use diazoxide preoperatively because it interferes with the intraoperative glucose monitoring. Frequent blood sugar determinations are necessary to prevent hypoglycemia during the operation. Our current protocol is to monitor blood sugar levels at 15- to 30-minute intervals both during the procedure and for several hours thereafter. A rise in serum glucose suggests that a curative operation has been performed. However, this is not always the case,...

What Other Psychiatric Symptoms May Develop In Epilepsy

Anxiety is an important and common condition associated with epilepsy and can have various causes. In addition to the direct anxiety produced by a seizure during the ictal phase, anxiety symptoms can develop during the postictal and interictal periods. Seizures can produce autonomic effects resulting in symptoms that mimic anxiety or panic, including increased heart rate, increased blood pressure, and flushing. In patients with epilepsy, anxiety may also develop as a response to anticipating a seizure, which could result in the development of secondary phobia. Certain medications (such as stimulants), medication withdrawal from barbiturates or benzodiazepines, and alcohol and substance abuse may also result in anxiety states. Various medical conditions, including thyroid disease, asthma, hypoglycemia, and adrenal dysfunction, may also produce anxiety. In summary, the clinician should consider all these potential causes when evaluating a patient with epilepsy in whom an anxiety...

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...

Laboratory Parameters

It is important to obtain a serum chemistry profile to help identify the underlying cause of SE. Abnormalities that can cause seizures include hypoglycemia, hyponatremia, hypernatremia, hypomagnesemia, hypocalcemia, and renal and liver failure. In a febrile patient with an elevated white blood cell count (WBC), an active infection should be ruled out or treated appropriately. Cultures from the blood, cerebrospinal fluid (CSF), respiratory tract, and urine should be obtained once the seizures are controlled. CT or MRI can be done to rule out CNS abscesses, bleeding, or tumors, all of which may be a source for seizure activity. A blood alcohol level and urine toxicology screen for drugs of abuse should also be conducted to determine if alcohol withdrawal, illicit drug use, or a drug overdose could be the underlying cause of SE. Also, drug levels should be obtained in a drug overdose situation to rule out

Acute Adrenal Insufficiency

During an acute adrenal crisis, the immediate treatment goals are to correct volume depletion, manage hypoglycemia, and provide glucocorticoid replacement. V lume depletion and hypoglycemia can be corrected by giving2large volumes (approximately 2-3 L) of IV normal saline and 5 dextrose solution. Glucocorticoid replacement can be accomplished by administering IV hydrocortisone, starting at a dose of 100 mg every 6 to 8 hours for 24 hours, increasing to 200 mg to 400 mg day if complications occur, or decreasing to 50 mg every 6 to 8 hours after achieving hemodynamic stability. The hydrocortisone dose can then be tapered to a maintenance dose by the fourth or fifth day and fludrocortisone can be added if needed.2

Clinical Manifestations

Most important of all, and underlying most of the symptoms - profound acidosis the latter, if untreated, leads to coma and death. Because of the acidosis, the breath smells of acetone, described in the past as an overpowering fetor. The weakness is thought to be due chiefly to hypoglycemia, and death, to ketoacidosis and marked fatty degeneration of the liver, kidney, and muscles. The disease can be chronic or latent, and is likely to recur if the patient is subjected to fatigue, starvation, intercurrent infection, or vigorous exercise.

Emergency Department Treatment and Disposition

Core temperature measurement is best made with an esophageal probe. Rectal temperature is less accurate without the use of a special low-reading thermometer. Gentle handling and appropriate warming methods are the mainstays of ED treatment. Cardiovascular instability often complicates rewarming Advanced Cardiac Life Support (ACLS) guidelines for hypothermia provide guidance. If not obvious, a cause should be sought (eg, hypothyroidism, hypoglycemia, sepsis), as should associated pathology. Most patients require admission for observation or to treat associated injuries or comorbidities.

Glycoprotein IIbIIIa Receptor Antagonists

In the setting of non-ST-segment elevation ACS, although the overall impact of GP IIb IIIa receptor inhibitors used in a conservative setting has been modest,119 a mortality benefit was detected among diabetic patients. Accordingly, the meta-analysis of the diabetic populations (n 6458) enrolled in the six large-scale trials of GP IIb IIIa inhibitors in ACS detected a highly significant 26 mortality reduction associated with the use of these agents at 30 days, compared with placebo (Fig. 2-15).120 These findings were reinforced by a statistically significant interaction between treatment and diabetic status. The use of these potent platelet inhibitors was associated with a similar proportionate reduction in mortality for patients treated with insulin and for those treated with diet or with oral hypoglycemic drugs. Even more striking was the mortality reduction (70 ) associated with the use of GP IIb IIIa inhibitors among the diabetic patients who underwent PCI (see Fig. 2-15).

Measurement of Proinsulin and C Peptide

There are two specific instances in which measurement of C peptide levels has been particularly helpful. The first is in patients with insulin-dependent diabetes mellitus. Such patients may have circulating antibodies to insulin that interfere with the measurement of insulin in the blood. Elevated levels of C peptide help confirm the diagnosis of insulinoma in such patients. The second situation in which the C peptide level is most useful is in patients who are surreptitiously injecting insulin. Commercial insulin has no C peptide thus, these patients have low levels of C peptide in the setting of a high insulin level and hypoglycemia.

Glucose and Insulin Levels

Currently, the diagnosis of insulinoma is confirmed by demonstrating a circulating insulin level that is inappropriately high for the serum glucose level, measured at the time of hypoglycemia (Fig. 79-3). When a patient presents with symptoms of hypoglycemia (i.e., coma, convulsions, or other neurologic symptoms), blood samples should be taken for the determination of both insulin and glucose levels. Samples should be drawn as early as possible to avoid complications of hypoglycemia and before treatment with glucose. Also, later, epinephrine secretion may cause mobilization of liver glycogen with a compensatory rise in serum glucose, possibly masking the hypoglycemia associated with an insulinoma. Although normal serum glucose levels are 60 to 95 mg dL, symptoms of hypoglycemia usually do not occur until levels are less than 50 mg dL. Normal serum insulin levels are typically below 30 pU mL.

Hospital Care of Diabetic Patients

Similar studies of glycemic control have not been definitive in critically ill patients with sepsis to GI bleeding, although these varying diagnoses may have created methodologic issues. Thus, professional societies are recommending that critically ill patients be maintained with glucose levels less than 140 mg dL (ADA, 2009). These therapeutic goals seem reasonable, until therapeutic methodology improves to limit hypoglycemia, which adversely affects outcomes associated with intensive insulin treatment protocols.

Cognitive Changes in Children With Type 1 Diabetes

Evidence suggests that children with type 1 diabetes may experience a wide range of cognitive difficulties associated with their disease. A number of studies document that these children are at risk for learning disabilities and may experience difficulties with attention, processing speed, long-term memory, and executive functioning (e.g., McCarthy et al. 2003 Rovet and Alvarez 1997 Schoenle et al. 2002). As a result, academic problems may emerge, particularly for those children who have earlier age at onset and who tend to have severe, recurring hypoglycemic episodes. Neurocognitive screening or a complete neuropsychological evaluation should therefore be considered for youth with type 1 diabetes, particularly for those who have experienced many negative glycemic events or who are struggling with school performance. Such an evaluation may well help the school develop an Individualized Education Plan that addresses needed academic and or physical accommodations.

Insulindependent diabetes mellitus

In healthy children, insulin levels decrease with exercise so that glucose can be liberated from stores in the liver and blood levels are maintained despite an increase in glucose uptake into the exercising muscle. Children suffering from insulin-dependent (type 1) diabetes mellitus have to inject insulin into the subcutaneous fat tissue. In consequence, insulin is liberated at a constant rate from the subcutaneous injection site, irrespective of glucose demand. Since insulin sensitivity increases during and following exercise, these children are at a high risk of experiencing severe hypoglycemia with exercise, resulting in a loss of consciousness or epileptic seizures. Low blood glucose levels have been described for up to 24 h following exercise in patients with insulin-dependent diabetes. In a survey of parents whose children had suffered from severe hypoglycemia, many parents blamed preceding exercise as trigger. Children should therefore be advised to measure blood glucose before...

Revascularization In Diabetic Patients With Stable Coronary Disease

Paralleling what was described for PCI, diabetes also negatively affects outcomes after CAbG. The impact of diabetes on morbidity and mortality in patients undergoing surgical coronary revascularization was addressed in a retrospective cohort study, based on the 1997 Society of Thoracic Surgery (STS) database, that included 41,663 diabetic patients among a total population of 146,786 patients.58 At 30 days, the mortality rate was significantly higher in the diabetes group (3.7 versus 2.7 ). The unadjusted and adjusted OR for mortality in these diabetic patients were 1.4 and 1.2, respectively. With respect to diabetes treatments at presentation, the adjusted OR for mortality among patients taking oral hypoglycemic drugs was 1.1, and that for patients taking insulin was 1.4. In addition, the overall morbidity rate and the infection rate were significantly higher in the diabetic patients. With respect to long-term mortality after CABG, a prospective New England cohort study that included...

Interpretation of the Fasting Test

It is essential to measure plasma C peptide at the end of the fast measurement of plasma proinsulin can also be helpful. Measurements of plasma C peptide distinguish endogenous from exogenous hyperinsulinemia. In patients in whom plasma glucose concentrations fall below 45 mg dL (2.5 mmol L), there is no overlap in the values in insulinoma patients and normal subjects at a plasma C peptide value of 0.2 nmol L. All insulinoma patients have higher values and all normal subjects who are hypoglycemic have lower values. For plasma proinsulin, the diagnostic criterion for insulinoma is 5 pmol L or greater.16

Clinical Presentation

An overt clinical syndrome of hypersecretion (60 of cases). Women younger than 40 years are more often affected. In patients with malignant adrenocortical tumors, the syndrome is of almost pure hypercortisolism in 30 of such cases, virilization in 22 , feminization in 10 , hyper-aldosteronism in 2.5 , and mixed secretions in 35 .1,12 Although adrenocortical carcinomas account for 5 to 10 of cases of hypercortisolism, 80 are due to corticotropin-secreting pituitary tumors. Notably, however, 40 of patients with Cushing's syndrome and adrenal neoplasms have malignant tumors. Virilizing tumors are malignant in 30 of cases, feminizing tumors in men are virtually always malignant, and pure aldosterone-secreting tumors are malignant in less than 1 of cases.14 Mixed secretion is highly suspicious of malignancy. Ectopic hyperinsulinism with hypoglycemia (Anderson's syndrome) or ectopic

Are Preoperative Localization Tests Beneficial

Intraoperative sonogram. A, Insulinoma of the tail of the pancreas. The arrows designate the insulinoma, which is hypoechogenic compared with the surrounding pancreas. B, A hypoechoic tumor (T) of the pancreas is visualized by intraoperative ultrasonography. Note that the pancreatic duct (arrow) and its proximity to the tumor are clearly shown. (A, From Kaplan EL, Arganini M, Kang S-J. Diagnosis and treatment of hypoglycemic disorders. Surg Clin North Am 1987 67 395-410. B, From Zeiger MA, Shawker TH, Norton JA. Use of intraoperative ultrasonography to localize islet tumors. World J Surg 1993 17 448.)

Hormonal regulation of carbohydrate metabolism during exercise

Changes in insulin and glucagon have been reported to account for practically all of the increase in hepatic glucose output with exercise 65,66 . It is believed that the decrease in insulin concentration with exercise makes the liver more sensitive to the stimulation by glucagon. Sympathetic nervous stimulation seems to have no role in stimulating hepatic glucose output during exercise in humans, whereas epinephrine has a stimulating effect, additional to that of glucagon, during prolonged exercise, when epinephrine levels are at their highest. In addition, cortisol has an indirect effect on hepatic gluconeogenesis, by increasing the enzymatic potential for this pathway. The catecholamines are important in 'sensitizing' skeletal muscle glyco-genolysis to the stimulating effect of contraction. With exercise leading to hypoglycemia, the compensatory increase in hepatic glucose output is mainly triggered by epinephrine 32 .

Clinical Trials Of Percutaneous Transluminal Coronary Angioplasty In Coronary Artery Disease

In the landmark Bypass Angioplasty Revasculariza-tion Investigation (BARI) trial,51 subjects with multi-vessel disease were randomly assigned to an initial treatment strategy of CABG (n 914) or PTCA (n 915), with a mean follow-up of 5.4 years. The 5-year survival rate was 89.3 for CABG patients and 86.3 for PTCA patients (P .19). The in-hospital event rates for CABG and PTCA were 1.3 and 1.1 , 4.6 and 2.1 for mortality for Q-wave MI (P < .01), and 0.8 and 0.2 for stroke, respectively. The 5-year survival rates free from Q-wave MI were 80.4 and 78 , respectively. At 5 years, 8 of the patients assigned to CABG had undergone additional revas-cularization procedures compared with 54 of those assigned to PTCA 69 of those assigned to PTCA did not subsequently undergo CABG. A key observation was that diabetics, who were treated with insulin or oral hypoglycemic agents at baseline, had a 5-year survival rate of 80.6 when treated with CABG, compared with a significantly lower survival rate...

Frequency of Complications

In a study of patients transferred to a rehabilitation center within a mean of 10 days after a stroke, the incidence of serious medical complications found upon admission rose from 22 before to 48 the year after institution of DRGs.18 Many of these complications derived from altering or starting medications during the acute hospitalization, especially antihyper-tensives, antiarrhythmics, platelet antiaggre-gants, anticoagulants, steroids, hypoglycemics, antibiotics, anticonvulsants, analgesics, and sedatives. Azotemia, hypoglycemia, hyponatremia, orthostatic hypotension, and a drug-induced encephalopathy were among the most common problems encountered. These problems delayed rehabilitative therapies and contributed to additional medical morbidity. Hyperglycemia hypoglycemia

Reviews and Selected Updates References

A large number of diseases, at least 70, involve the metabolism of organic and amino acids. Some diseases present as repeated episodes of acute metabolic decompensation, and the central nervous system (CNS) involvement is usually secondary to the accompanying acidosis, hypoglycemia, or hyperammonemia or to the elevated concentration of amino acids. Nevertheless, it is the secondary involvement of the CNS that is important and is the main problem requiring management. Another group of these disorders involves the CNS primarily, with the systemic disease being negligible. Such disorders are difficult to label at the time of initial encounter as either an organic or amino acid disorder because there are no episodes of acid-base disturbance or disturbance of glucose or ammonia metabolism. They can only be diagnosed by specialized biochemical tests. The recent advent of tandem mass spectrometry is changing the practice of neurometabolic diseases since it provides a rapid diagnosis. i , y...

Lethal Infantile Mitochondrial Disease or Congenital Lactic Acidosis

Supportive treatment of liver, renal, and cardiac failure is important, along with consultation with a center using experimental protocols. For respiratory chain defects, megadoses of vitamins K and C, coenzyme Q10, L-carnitine, and folic acid have all been tried with controversial benefit. If PDH deficiency is the cause, thiamine and lipoic acid may be therapeutic, because PDH requires these as cofactors. If biotinidase deficiency or multiple carboxylase deficiency is the cause, 50 mg of biotin daily can be given. Fructose-1,6-biphosphatse deficiency and glucose-6-phosphatase deficiency, both gluconeogenic defects, respond to frequent daily and continuous nocturnal feedings to prevent hypoglycemia. There is no effective treatment for pyruvate carboxylase deficiency or partial defects of the Krebs cycle. Correction of the metabolic acidosis and lowering of serum lactic acid is most effective with sodium dichloroacetate (DCA), 15 to 200 mg kg day administered intravenously or orally....

Fatty Acid Oxidation Disorders

In these disorders there are three main presentations (1) acute toxic encephalopathy with episodes of nonketotic hypoglycemia in the first 2 years of life provoked by fasting (MCAD), (2) skeletal and or cardiac myopathies with weakness (carnitine palmitoyl transferase CPI I and II deficiencies, LCAD, LCHAD, SCAD) and low plasma carnitine, and (3) the syndrome of nonketotic hypoglycemia plus very low plasma carnitine levels (< 10 pM) and absent dicarboxylicaciduria (carnitine transport defect). Ihe general

Directed Neurological Examination Overview

The examination of the patient with altered consciousness begins by ensuring that the patient's vital signs and basic biochemistry are adequate to support brain function. It is essential to ensure that blood pressure, respiration, and oxygen saturation are adequate and that the patient is not hypoglycemic or thiamine deficient before proceeding with the examination outlined later. In many situations (e.g., emergency departments), naloxone is also administered at this point to reverse any putative effects of opiates. The empirical use of flumazenil to antagonize potential benzodiazepine intoxication as a routine measure is controversial because of the risk of provoking seizures or status epilepticus, especially in patients with mixed benzodiazepine and cyclic antidepressant overdoses.

Carnitine Transport Defect Primary Generalized Carnitine Deficiency

Carnitine fails to be taken up in muscle, heart, and kidney but not liver, leading to insufficient carnitine to support fatty acid oxidation. Ihe kidney fails to conserve carnitine by reabsorption, resulting in very low plasma carnitine levels, which then causes decreased passive diffusion into liver, impairing ketogenesis. Accumulating acyl-CoA compounds become substrates for peroxisomal beta- oxidation, which produces medium-chain fatty acids and dicarboxylic acids, which do not require carnitine for mitochondrial entry. They are then completely oxidized in mitochondria, which is the reason for lack of dicarboxylicaciduria in disorders of the high-affinity carnitine transporter. Treatment with L-carnitine restores plasma levels to normal (40 to 60 pM) but not skeletal muscle. Muscle function can be restored, however, with less than 10 percent normal muscle carnitine levels. This is a rare disorder, and the exact incidence is unknown. Ihere are two major types of presentation, an...

Carnitine Palmitoyl Transferase II Deficiency

Ihere are two presentations the adult muscular form, in which prolonged exercise induces weakness and myoglobinuria, and a severe infantile form, in which nonketotic hypoglycemic coma without dicarboxylicaciduria, seizures, hepatomegaly, cardiomegaly, and cardiac arrhythmia are accompanied by low plasma and tissue levels of carnitine with increase in long-chain acylcarnitines. Ihe classic adult form is autosomal recessive and usually affects males between 15 and 30 years of age. Ihe serum creatine kinase value is normal between episodes, carnitine levels are usually normal in plasma and tissues, and long-term muscle weakness is rare, although lipid storage may be seen on muscle biopsy. Ihe differential diagnosis includes other carnitine cycle disorders. Management involves supportive treatment of the renal failure and measures to remove the myoglobin from kidney and avoidance of triggering factors-prolonged exercise, exposure to cold, infections, and fasting. Presentation in the...

The Biopsychosocial Model

Changes in relation to a patient's emotional patterns, life goals, attitudes toward illness, and social environment. Engel proposed that the brain and peripheral organs were linked in complex, mutually adjusting relationships, affected by changes in social as well as physical stimuli. Within this model, environmental and psychological stress is seen as potentially pathogenic for the individual. Emotions may serve as the organism's bridge between the meaning (or significance) of stressful events and the changes in physiologic function (Zegans, 1983). Engel urged physicians to evaluate the patient on biologic, psychological, and social factors in order to understand and manage clinical problems effectively (Wise, 1997). For example, a workplace accident could be seen as resulting from poorly designed equipment (social) and inattentiveness (psychological) brought about by low blood sugar (biologic). Similarly, the accident could result in damage to internal organs (biologic), distress...

Posterior Pituitary Disorders

The biologic effects of AVP are initiated at two receptors, V1 and V2. The V1 receptors are located in the vascular system, and their stimulation results in vasoconstriction. The V2 receptors are located in the kidneys, and their stimulation results in free-water reabsorption (Korbonits and Carlsen, 2009). Plasma osmolality, blood volume, and blood pressure are the most important physiologic stimuli of AVP secretion. Other factors that modulate AVP secretion include pain, stress, nausea, hypoglycemia, hypercapnea, angiotensin II, atrial natriuretic hormone, and drugs. Many stimuli of AVP release also promote thirst. Thirst is less sensitive than AVP release in response to these stimuli and therefore is a second-line defense against dehydration.

Hypertension

ACE inhibitors or angiotensin receptor blockers (ARB), often in combination with a thiazide diuretic, should be considered as initial therapy (Table 2-10). The use of P-blockers in diabetic patients with CAD is associated with improved survival, even in those without a previous MI. Therefore, in this subgroup of patients, P-blockers and the combination of P-blockers and ACE inhibitors are considered the regimens of choice. It should be emphasized that P-blockers are not contraindicated in diabetic subjects with impaired hypoglycemia awareness, nor in those with PAD, particularly if cardioselective P1-blockers are used. With respect to calcium channel blockers, dihydropyridines have been shown to decrease cardiac events and stroke, whereas nondihy-dropyridines reduce the progression of diabetic nephropathy.131 Because randomized trials have

Glucose

The reference range for a fasting plasma glucose level is between 70 and 99 mg dL. Hypoglycemia is best documented by a plasma venous glucose level less than 50 mg dL, although there is considerable variability in the level of hypoglycemia that causes symptoms. Asymptomatic hypo-glycemia in a patient not taking insulin or oral hypoglyce-mic agents may be a laboratory artifact caused by ongoing metabolism of glucose in the specimen, especially if a delay has occurred in processing the specimen. The diagnosis of hypoglycemia is best made with typical symptoms associated with a laboratory confirmation of venous hypoglyce-mia, followed by relief of symptoms after ingesting glucose. The glucose tolerance test (GTT) can produce hypoglycemia in normal persons and should not be routinely ordered in the evaluation of hypoglycemia. Hypoglycemia can be defined as iatrogenic, postprandial, or fasting. Postprandial hypoglycemia occurs after meals and is usually mild and self-limiting. Alimentary...

Initial Treatment

All patients should receive glucose in case of hypoglycemia-induced SE. In patients with a history of alcohol abuse, thiamine 100 mg should be given prior to the administration of any glucose-containing solutions to prevent encephalopathy Once the first dose of benzodiazepine is given, an AED should be started to prevent further seizures from occurring. If the underlying cause of the seizures has been corrected (e.g., hypoglycemia) and seizure activity has ceased, an AED may not be necessary. AEDs must not be given as first-line therapy because they are infused relatively slowly to avoid adverse effects, delaying their onset of action.

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.

Jitteriness

Jitteriness is defined as rhythmic tremors of equal amplitude and is frequently seen in the healthy infant. These tremors can be easily initiated in the susceptible newborn by external stimuli such as handling or loud noise. One can stop the tremor by gently holding the affected extremity. Although jit-teriness often occurs in the healthy infant, tremors may be a manifestation of a variety of neonatal problems, including hypoglycemia, hypocalcemia, drug withdrawal from maternal drug use, and perinatal asphyxia. In the infant with persistent or exaggerated tremors, possible causes must be investigated (Hoekelman, 2001).

Clinical History

One of the first questions to address in the history is whether the problem involves neurovascular dysfunction. The clinical hallmark of many forms of neurovascular dysfunction is an acute focal change in neurological status. Therefore, an event that has an indistinct onset or course may not involve the neurovascular system. There are two exceptions to consider. One is the indistinct time of onset of symptoms in an individual who awakens with the neurological dysfunction. The other is a stuttering or waxing or waning course that can be seen in some patients with cerebral arterial thrombosis. In most instances of neurovascular dysfunction, the neurological deficit is maximum from its onset, with the involved body parts being simultaneously affected. The diagnosis of neurovascular dysfunction is weakened if there is a series of events in which neurological deficits accumulate, or if there is a march of symptoms from one area to another. Focal seizures can usually be differentiated by...

Disease and Enzymes

Test findings should be grouped into two age categories one for neonatal and one for episodes after 6 months of age. In the neonatal period, the disease almost never causes significant hypoglycemia, nor acidosis, ketonuria, or hyperammonemia. Therefore, the presence of coma in a neonate who has nearly normal clinical biochemical findings should immediately suggest MSUD. Definite diagnosis is through determination of amino acids in plasma or in urine, which shows significant elevations of L-leucine, isoleucine, and valine. Leucine concentration in blood is always higher than that of the other BCAAs. BCAAs or BCKAD can be measured either by chromatographic techniques or more rapidly by tandem mass spectrometric determinations. A quick spot test of the BCKA in the urine is a strongly positive yellow flocculation when 2,3- dinitrophenylhydrazine is added. After 6 months of life, when recurrent acute metabolic decompensation occurs, it is accompanied by mild to moderate...

Etiology

Amenorrheic athletes often have slightly elevated Cortisol levels, as do women with FHA or anorexia nervosa. Cortisol is a glucoregulatory hormone activated by low blood glucose levels 36 . Cortisol levels have found to be elevated in both FHA and exercise-associated amenorrhea.

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)....

Advice on Alcohol

What constitutes a drink Either a 12-ounce beer, a 5- to 6-ounce glass of wine or 11 ounces of a distilled spirit like gin or rum. It's very important that alcohol be consumed with food in order to reduce the risk of hypoglycemia, or low blood sugar. And when calculating your daily food plan, don't forget to count the alcohol as part of the day's calories.

Glucose Monitoring

Monitoring behavior is itself therapeutic because it warns of the risk of hypoglycemia or a shift to a hyperglycemic state caused by dietary indiscretion or a smoldering stress. Glu-cometers are now available that require less than 1 L of blood (taken up by capillary action). A sample may be taken from a fingertip, earlobe, forearm, or thigh, with the result available in 5 to 15 seconds. Arm or thigh values are derived from interstitial glucose concentration and may be approximately 15 minutes out of phase with blood values if the patient is not in a fasting steady state. Average monitored values over 14 to 30 days correlate with HbA1c values. Monitored glucose data are also the basis of formulating therapeutic targets. For a young girl with diabetes, the fasting target may be 150 mg dL to avoid early-morning hypoglycemia. As she matures, the target becomes the current American Diabetes Association (ADA) goal of less than 120 mg dL fasting and before meals. In elderly diabetic...

Glycemic Targets

Similar data from other large trials indicate that the difference in intensive efforts to lower HbA1c to values below 6 versus conventional treatment was not associated with reduced cardiovascular events in middle-aged type 2 diabetic patients (ACCORD, 2008 VADT, 2009). This may have resulted from unawareness of hypoglycemia common in patients with HbA1c values approaching 6 . Recurrent hypoglycemia may downregulate appropriate physiologic response to the stress of cardiac ischemia, which may be clinically silent in diabetic patients. with rapid onset of infection. Glycemic targets of 7 or less are ideal if attained without the risk of hypoglycemia unawareness.

Diabetic Retinopathy

Measures to prevent diabetic retinopathy include maintenance of glycemic control with avoidance of the stress of hypoglycemic reactions and control of blood pressure (BP). Aspirin therapy does not exacerbate or predispose to bleeding. However, intensive physical activity (exercise, sexual intercourse) can promote ocular bleeding.

Hepatic Failure

Clinical Features and Associated Disorders. The neurological manifestations of HE range from subtle psychomotor abnormalities to coma and death. The exact clinical picture depends on the rapidity of onset, the degree of liver dysfunction, and the degree of portal-systemic shunting. PSE, the much more commonly encountered form, is mostly observed among patients with chronic liver disorders (e.g., cirrhosis). In addition to the neurological features, these patients may have numerous other clinical findings (l Table ,38-13 ). PSE is typically precipitated by ammonia-producing processes, such as GI bleeding, increased dietary protein, constipation, and azotemia. Other known precipitants include infection, hypokalemia, hypoglycemia, hypoxia, and medications (e.g., sedative-hypnotics, analgesics). 137 Usually, the onset of encephalopathy is slow and insidious, often beginning with anxiety, altered sleep patterns and mood, agitated delirium, or a decreased attention span. Eventually,...

Hormone Receptors

The objective of pharmaceutical research is to discover and develop new substances that can be characterized by their selectivity and specificity. Selectivity describes the particular effects on physiological or pathological states that the substance can produce. These descriptions, such as hypnotic, hypoglycemic, hypotensive, and anti-inflammatory, may be wholly empirical however, this does not impede their therapeutic utility. Thus, the clinical utility of drugs such as morphine and digitalis was established long before we had biochemical explanations for their actions. Specificity, on the other hand, refers to the biochemical hypotheses that claim to explain the selectivity of a substance. Thus, activation of enkephalin receptors is proposed as the mechanism by which morphine acts, and inhibition of Na+- K+-dependent ATPase has been claimed to specify the activity of digitalis. All kinds of biochemical events have been used to specify drug actions. Interactions with enzymes, ion...

Hyperglycemia

Similar results were documented among patients after myocardial infarction 30 . The question remains regarding the application in acute stroke patients. The GIST-UK trial 31 addressed this question. The study was conducted among 933 hyper-glycemic acute stroke patients who received glucose-potassium-insulin infusion versus placebo. In the treatment group significantly lowered glucose and blood pressure values were documented however, no clinical benefit was found among the treated patients. The time window for treating post-stroke hyperglycemia still remains uncertain. There are a variety of methods of insulin administration, including continuous intravenous (i.v.) infusion, repeated subcutaneous dosing and i.v. infusion containing insulin and dextrose with potassium supplementation 32 . Ongoing trials address the role of i.v. insulin for hyperglycemic stroke patients. The Glucose Regulation in Acute Stroke Patients Trial (GRASP) is continuing recruitment. Patients...

Signs and Symptoms

The symptoms of an insulinoma are based on profound hypoglycemia with a lack of glycogen in the brain but also are due to the release of epinephrine secondary to a low serum glucose level. The signs and symptoms are best classified The diagnosis of insulinoma is often delayed and can take as long as several months to years, depending on the severity of symptoms and frequency of hypoglycemic attacks. Delays in diagnosis are due in part to the variability and severity of the clinical presentations but certainly depend on physician awareness as well. The attacks are usually associated with fasting most commonly, they occur before breakfast and during the late afternoon. However, attacks of fasting hypoglycemia may occur during exercise as well. It must be understood that the severity of the clinical presentation predicts neither the size nor the malignant potential of the insulinoma. FIGURE 79-2. Secretion of insulin from the pancreatic islet beta cells Schema of rough endoplasmic...

Fasting Test

As most patients with an insulinoma have intermittent attacks, the physician is unlikely to see patients while they are acutely hypoglycemic. The most reliable method for documenting a hypoglycemic episode is the prolonged fasting test. This is the gold standard of testing. After baseline circulating insulin and glucose levels are obtained, the patient fasts for 72 hours or until hypoglycemic symptoms occur. Serum glucose levels are checked at regular intervals, usually every 1 to 2 hours and more frequently when the glucose level falls below 50 mg dL. Simultaneous insulin levels are obtained with the onset of symptoms or if the glucose level falls below 50 mg dL. FIGURE 79-4. Levels of plasma insulin and blood glucose during the last 4 hours of a 12-hour fast in a patient with an insulinoma. (From Kaplan EL, Arganini M, Kang S-J. Diagnosis and treatment of hypoglycemic disorders. Surg Clin North Am 1987 67 395.)

Provocative Tests

Glucagon stimulates the release of glucose from liver glycogen stores, thereby producing a rise in blood glucose levels. A baseline glucose level is obtained, and then 1 mg of glucagon is injected intramuscularly. Serum glucose levels are then obtained at 15 minutes, 30 minutes, and subsequent 30-minute intervals for 3 hours. Normally, there is a rapid rise in serum glucose levels during the first hour, with a return to fasting glucose levels by 3 hours. Reactive hypoglycemia does not occur. In the presence of an insulinoma, however, there is a greater than normal rise in the glucose levels, followed by severe hypoglycemia in the presence of elevated levels of insulin. This test is positive in 72 of patients with insulinomas. A glucose tolerance test may also indicate the presence of an insulinoma. Fifty grams of glucose in 100 mL of water is given orally and serum glucose levels are measured at 0, 30, 60, 90, 120, and 180 minutes. Normally, the peak glucose level is reached by 1...

Step

Patients with psychogenic seizures frequently present to neurologists or epilepsy monitoring units having been diagnosed with epilepsy and treated with anticonvulsants. Seizures may be difficult to differentiate from frontal lobe seizures characterized by violent motor activity and sexual automatisms. Malingering and physiological nonepileptic events such as cerebral hypoperfusion, hypoxia, hypoglycemia, electrolyte disturbances, alcohol and drugs effects, migraine, gastroesophageal reflux, parasomnias, and movement disorders including paroxysmal dyskinesias may produce similar symptoms.

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.

Islet Cell Tumors

Endocrine tumors of the pancreas are rare and arise from the normal elements of the pancreatic islets. Insulinoma is the most common islet cell tumor followed by gastrinoma. As shown in Table 88-1, its primary symptom is hypoglycemia. Histologic criteria of malignancy, such as cytologic atypia, angioinvasion, and perineural invasion, are often absent, even in metastatic islet cell tumors.7 The only universally agreed-on proof of malignancy is infiltration of adjacent organs and spread to distant sites.8 Only 10 to 15 of insulinomas are malignant.9 In contrast, 60 of islet cell tumors producing gastrin10 or vasoactive intestinal polypeptide (VIP)11 are malignant. The characterization of islet cell tumors by plasma or hormone production provides important prognostic information. Hypoglycemia The incidence of insulinoma is generally considered to be 1 per 1,000,000 to 1,250,000 people, but it may be up to 4 patients per 1 million individuals per year.12 Approximately 75 of insulinomas...

Oral Agents

Hepatorenal clearance Hypoglycemia Hepatic clearance Hypoglycemia Sulfonylureas are insulin secretogogues that can be used as first-line drugs or in combination with any of the oral medications. An important advantage is their low cost. However, diabetic patients who do not demonstrate fasting hyperglyce-mia have an increased risk of hypoglycemia if HbA1c is being maintained below 7 . Another hypoglycemic risk is renal disease, which reduces gluconeogenesis and permits typical sulfonylureas such as glyburide and glipizide to accumulate. Glimepiride and the meglitinides may be used in mild azo-temia because of their greater hepatic excretion. The meg-litinides are nonsulfonylurea secretogogues that activate a different K+ channel. The meglitinides are theoretically safer in elderly patients because of their short half-life, although treatment is required before all meals. Their disadvantage is that generic preparations are not yet available. Failure to respond to metformin is an...

Palpitations

In addition to primary cardiovascular causes, thyrotoxicosis, hypoglycemia, fever, anemia, pheochromocytoma, and anxiety states are commonly associated with palpitations. Hyperthyroidism is an important cause of rhythm disturbances that originate outside the cardiovascular system. Caffeine, tobacco, and drugs are also important factors in arrhyth-mogenicity. Sympathomimetic amines used in the treatment of bronchoconstriction are potent stimuli for arrhythmia as well. In patients with panic disorders and other anxiety states, the sensation of palpitations may occur during periods of normal rate and rhythm.

Generalized Seizures

TCS are observed in patients with idiopathic and symptomatic epilepsies and in association with systemic disease. 6J Hyponatremia, hypoglycemia, alcohol withdrawal, and drugs are common causes of isolated seizures particularly in hospitalized patients. Drugs that may precipitate TCS include tricyclic antidepressants, antipsychotics, anticholinergics, antihistamines, methylxanthines, antibiotics, and withdrawal from barbiturates and benzodiazepines. The prognosis for patients with idiopathic generalized TCS is better than that for those with focal or secondary generalized seizures, which tend to persist if untreated. The remission rate is greatest in patients who develop TCS in childhood in the absence of other seizure types.

From Ftef

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. An individualized meal plan consisting of three meals and three snacks per day is commonly recommended in GDM. Preventing ketosis, promoting adequate growth of the fetus, maintaining satisfactory blood glucose levels, and preventing nausea and other undesired GI side effects are desired goals in these patients. Controlling blood sugar levels is important to prevent harm to the baby. An abundance of glucose causes excessive insulin production by the fetus which, if left uncontrolled, can lead to the development of an abnormally large fetus. Infant hypoglycemia at delivery, hyperbi-lirubinemia, and complications associated with delivery of a large baby also may occur when blood glucose levels are not controlled adequately. H hypoglycemia occurs,...

Myxedema Coma

Decreased mental function is an important feature of myxedema coma. Lethargy, stupor, confusion, and psychiatric symptoms may precede the coma. The causes of the altered mental status and CNS decompensation in patients with severe thyroid hormone deficiency include hyponatremia, carbon dioxide (C02) narcosis, hypoglycemia, postictal mental disorder, and coexistent sepsis or hypoadrenalism. Administration of sedatives and tranquilizers may further suppress the CNS because the clearance of drugs is markedly retarded in hypothyroid patients. Heat production by brown adipose cells is stimulated by catecholamines through a-adrenergic receptors and modulated by thyroid hormone. Hypothermia is commonly encountered in myxedema coma and may precede the development of coma. The body temperature may be as low as 24 to 34 C and often cannot be recorded by the usual thermometer. Hypothermia is due to severe hypometabolism, adaptive peripheral vasoconstriction, and relatively unopposed (...

Adrenal Disorders

Clinical Features and Associated Disorders. The clinical features of adrenal insufficiency are influenced by the site of dysfunction, because PAI affects all of the adrenocortical hormones, whereas SAI only affects glucocorticoids. Thus, hyperpigmentation, salt craving, and hyperkalemia are unique to patients with PAI. Patients with adrenal insufficiency may present acutely or as a chronic condition. Acute adrenal insufficiency is a medical emergency (so-called addisonian crisis) characterized by mental status changes, fever, hypotension, volume depletion, arthralgias, myalgias, and abdominal pain that may mimic an acute abdomen. yi Chronic adrenal insufficiency may present more insidiously with fatigue, weakness, GI symptoms, amenorrhea, decreased libido, salt craving, arthralgias, and hypoglycemic symptoms. Neurological manifestations can include confusion, apathy, depression, psychosis, paranoia, and myalgias, as well as hypoglycemic symptoms. 102 In addition, a past medical...

Pathophysiology

The pathophysiology of an insulinoma is based on excessive secretion of insulin, which results in the clinical presentation of hypoglycemia. During the 1960s, insulinomas and other endocrine tumors of the gastrointestinal tract were found to share common cytochemical characteristics as well as a common neuroectodermal origin. This diverse group of tumors was thus classified under the amine precursor uptake and decarboxylation (APUD) concept.7 Although the APUD concept is no longer accepted in its entirety, it played a very useful role at the time by allowing an explanation for the association of insulinomas with other neuroendocrine tumors under MEN 1. MEN 1 has now been definitively linked to a loss of heterozygosity on chromosome 11 (1 lql3).8 The gene for this disorder, called menin, has been described. In MEN 1, insulinomas are often associated with hormone-secreting tumors of the parathyroid, pituitary, adrenal cortex, and thyroid glands. In such patients, a variety of symptoms...

Diabetes

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...

Reyes Syndrome

Evaluation and Differential Diagnosis. Laboratory studies during the prodromal phase are not diagnostic. Once vomiting develops, alanine aminotransferase and aspartate aminotransferase levels are often very high, often 20 to 30 times normal, but ammonia levels are in the normal range. As coma develops, ammonia levels increase threefold or more over the normal range. Other abnormalities of laboratory tests occur with increases in lactic acid and organic acids, suggesting a blend of respiratory alkalosis and metabolic acidosis, sometimes with hypoglycemia, especially in children younger than 3 years of age. Prolonged prothrombin times develop, but hemorrhaging is rare. The EEG is abnormal with diffuse slowing, and sometimes, burst suppression activity (see Chapter 24 ), but there is no specific pattern of diagnostic value. Liver biopsy shows highly characteristic fatty metamorphosis without inflammation. Neuroimaging with CT or MRI shows a normal brain or diffuse cerebral edema with...