New Home Remedies 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! Read more...

Guide To Beating Hypoglycemia Summary

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Etiologies of Hypoglycemia

Drug-induced Oral hypoglycemic agents, par-enteral insulin preparations. Food or drug potentiation of hypoglycemic agents Foods (unripe Jamaican ackee fruit-hypoglycin vomiting, hypoglycemia, CNS depression, seizures , ethanol) drugs (ACE inhibitors, P-blockers, chloramphenicol, diso-pyramide, MAOIs, quinine-quinidine, salicy-lates, sulfonamides).

Overview and Summary of Oral Hypoglycemic Agents

The four classes of oral hypoglycemic agents currently used to treat T2DM facilitate glycemic control via separate mechanisms (Table 6 and Figure 7). The insulin secretagogues (sulfonylureas and meglitinides) act on pancreatic b-cells to increase insulin secretion and bioavailability. Biguanides suppress excessive hepatic glucose production and improve hepatic insulin action. Thiazolinediones improve peripheral insulin sensitivity, especially in muscle and adipose tissues. a-Glucosidase inhibitors delay gastrointestinal absorption of dietary glucose, decreasing postprandial glucose excursions. Each class can be used as monotherapy or in combination.

Hypoglycemic Encephalopathy

A 68-year-old diabetic man, following administration of 11 units regular insulin, suffered a hypoglycemic episode with a blood glucose concentration of 28 mg 100 mL for approximately 8 hours. During this episode, he became comatose and, without regaining consciousness, died 15 days later. Eosinophilic neurons and mild astrocytosis (HE) are present in the thalamus. The clinical presentation varies with the severity and duration of hypoglycemia. It ranges from headaches, perspiration, nervousness, and tremulousness through confusion, myoclonic jerks, and seizures, to decerebrate rigidity and coma leading ultimately to death. Those who survive a severe and prolonged hypo-glycemic episode usually are left with variable cognitive deficits and various neurologic symptoms and signs. Similarities and differences can be seen between the pathogenesis and pathology of hypoglycemic and isch-emic-hypoxic encephalopathies. In both conditions, the neurons are affected...

Hypoglycemia

Oversecretion of insulin in response to meals produces a disorder termed reactive hypoglycemia. In reactive hypoglycemia meals rich in simple sugars and refined carbohydrates stimulate a large insulin response the insulin then pushes down blood glucose to below normal levels.16 Symptoms most often occur mid-morning and mid-to-late-after noon, usually 2-4 hours after eating a carbohydrate-rich meal. Because the brain depends on a steady supply of glucose, hypoglycemia impairs mentation, alertness, and concentration. Reactive hypoglycemia may cause fatigue and irritability. Reactive hypoglycemia can produce the following symptoms

Diet Hypoglycemia

A diet plan to reduce reactive hypoglycemia should include The glycemic index measures a food's potential to rapidly elevate blood glucose. If vulnerable to reactive hypoglycemia, foods with a high glycemic index may stimulate insulin oversecretion and trigger low blood sugar. These foods should therefore be avoided in favor of foods with a low to moderate glycemic index.

Figure 15 Structure of the cofactor uridine5diphosphoaDglucuronic acid 39 UDPGA generic reactions of O and

Another major group of substrates are alcohols, be they primary, secondary, or tertiary (Figure 15a). Medicinal examples include oxazepam (UGT1A9, 2B7, and 2B15) and zidovudine (36, Figure 14 UGT2B7). Another important example is that of morphine (41, Figure 16), which is conjugated on its phenolic and secondary alcohol groups to form the 3-O-glucuronide (a weak opiate antagonist) and the 6-O-glucuronide (a strong opiate agonist), respectively.82 Hydroxylamines and hydroxylamides may also form O-glucuronides (Figure 15a). Thus, a few drugs and a number of aromatic amines are known to be N-hydroxylated and then O-glucuronidated. A recent example has been found in the metabolism of a new oral hypoglycemic agent purine.83 When administered to monkeys, more than half of a dose was recovered as a compound found to be the O-glucuronide of the N-hydroxylated metabolite (42, Figure 16).

Abortifacients Compound Q

Compound Q is an herbal preparation of the Chinese Trichosanthin plant, which can inactivate viral ribosomes and inhibit HIV replication. Pharmacology Poor oral availability and intense diarrhea on oral administration severe biphasic neurotoxicity on parenteral administration. Toxicity CNS > dermatologic (hypersensitivity and anaphylaxis) > metabolic (hypoglycemia) CNS (1) Encephalomyelitis in 24-72 hours with fever, delirium, dementia, myalgias, paresis (2) coma within 1 week. Treatment Immediate ipecac on observed ingestion, lavage and activated charcoal (AC), supportive.

Regulators of Vascular Endothelial Growth FactorA and Vascular Endothelial Growth Factor Receptor Expression

VEGF-A expression by tumor cells is upregulated by multiple stimuli, including cytokines, growth factors, hypoxia, and hypoglycemia in addition to activation of oncogenes and mutation of tumor suppressors. The mechanisms by which VEGF-A levels are induced by hypoxia have been extensively elaborated. In normoxic conditions the transcription factor HIF-1a is maintained at low levels, due to the action of the von Hippel-Lindau tumor suppressor (VHL) which directs its ubiquitinylation and proteosome mediated degradation. Hypoxia results in stabilization of HIF-1a, permitting activation of target genes that includes VEGF-A, as well as proteases and adhesion molecules.238,239 Many cancers are characterized by areas of hypoxia, and an association between hypoxia or HIF-1a levels in primary tumors and probability of metastasis has been clinically established.254 In agreement, experimental manipulation of VHL or HIF-1a activity is associated with changes in tumor growth, vascularization, and...

Isopropanol Pharmacology and Toxicity

CNS Three times more CNS depression than EtOH, lethargy, weakness, headache, ataxia, dysarthria, confusion, apnea, respiratory depression, hypotension. Pulmonary and gastrointestinal Acetone breath, hemorrhagic gastritis and hemor-rhagic tracheobronchitis. Metabolic Exception only toxic alcohol not causing metabolic acidosis or hypoglycemia euglycemia is maintained ketonemia and ketonuria occur from acetone poisoning.

Measurement of symptoms

Most symptoms experienced during hypoglycaemia are considered to be generated either by the direct effects of low blood glucose on the brain (neuroglycopenia) or through activation of the autonomic nervous system. Both the sympathetic and parasympathetic divisions of the autonomic nervous systems are activated, causing direct neural stimulation of end-organs, and the magnitude of the responses may be augmented by profuse secretion of adrenaline from the adrenal medulla (McAulay et al. 2001).

PAdrenergic Physiology

There are three (3) types of p-receptors P1, P2, and p3, with p1 subserving the cardiovascular effects of increasing cardiac contractility, intra-cardiac conduction velocity, cardiac automatic-ity, and renal renin secretion. Specific p1-receptor stimulation causes the cardiovascular effects of increased cardiac contractility, intracardiac conduction velocity, cardiac automaticity, and renal renin secretion. Specific p2-receptor stimulation causes peripheral arteriolar vasodilation, pulmonary bron-chodilation, hepatic gluconeogenesis, and glycogenolysis, increased insulin secretion with hypoglycemia, and increased uptake by muscle resulting in serum hypokalemia. p3-receptor stimulation probably mediates ther-mogenesis and lipolysis.

Differential Diagnosis Drug Induced Bradycardia

High anaphylaxis risk Nonselectives block catechol's ability to reduce mast cell degranulation in patients with atopic allergies. Hypoglycemia All -blockers mask sympathetic response to hypoglycemia and interfere with gluconeogenesis glycogenolysis. Withdrawal Rebound increased heart rate and elevated blood pressure on abrupt withdrawal can precipitate MI and CVA.

Inducers Of Apoptosis Exist In The Ad Brain

Apoptosis can be induced in most neurons by a variety of stimuli, a number of which appear to accumulate in the aging and AD brain. In the aging and AD brain, the P-amyloid protein (AP), a 40-42 amino acid peptide, accumulates in the extracellular space as small deposits and senile plaques. Based on the observation that neurites surrounding AP deposits show both sprouting and degenerative responses, we proposed that this peptide is not metabolically inert, but rather possesses biological activity. Our findings established two key principles that AP induces neurotoxicity in a conformation-specific manner and that apoptotic mechanisms underlie this toxic-ity (1,2) these observations have since been confirmed by many others. Interestingly, prior to causing cell death, AP also induces the formation of dystrophic-like neurite morphology in cultured neurons (3,4). Oxidative insult readily initiates apoptosis (5), which is known to occur in the aging and AD brain (6). Similarly, reductions...

Basic Concepts for Assignment of the Reference Range

The use of the normal range as the reference range for interpretation of laboratory tests is appropriate when the analyte is used to determine multiple disease processes, abnormalities, or etiologies. Glucose is used to determine stress, diabetes mellitus, hypoglycemia, and other clinical conditions. Serum creatinine is generically used to indicate glomerular disease, irrespective to the underlying etiology (e.g., nephrotic syndrome or glomerular nephritis).

Of Antidepressant Treatments

This hypothesis could also explain the individual variability and susceptibility to stress-induced affective illness. Prior exposure of an individual to stress or some other type of neuronal insult, such as hypoxia-ischemia, hypo-glycemia, or infection, could induce a relatively small degree of neuronal damage that is not sufficient to result in behavioral abnormalities. However, with subsequent exposures to stress or environmental insults over time, the damage to neurons may be cumulative and eventually lead to illness. This type of scenario is observed in Parkinson's disease, where up to 80 of the substantia nigra dopamine neurons are lost before the illness is expressed. It is also possible that there are genetic factors involved that increase the vulnerability hippocampal neurons to stress.

Benefits of Glycemic Control

Intensive therapy reduced the risk for developing retinopathy by 76 (primary prevention) and slowed progression of pre-existing retinopathy by 54 , the incidence of severe retinopathy by 47 , and the need for laser therapy by 56 (secondary prevention). In the primary prevention cohort, the appearance of neuropathy was reduced by 69 at 5 years in subjects on intensive therapy compared with subjects on conventional therapy. In the secondary prevention cohort, intensive therapy reduced the appearance of clinical neuropathy at 5 years by 57 . Furthermore, intensive therapy prevented the development and slowed the progression of diabetic kidney disease by 50 . Intensive therapy, however, was associated with greater weight gain (about 1 kgyear _ 1) and a threefold greater risk of severe hypoglycemia (loss of consciousness or need of second person assistance) compared with conventional therapy.50 Similarly to the DCCT, the UKPDS found that a reduction in HbA1C resulted in decreased...

AGlucosidase inhibitors

Hypoglycemia in acarbose- or miglitol-treated subjects must be treated with simple carbohydrates found in milk, juices, or glucose tablets. Disaccharides or polysaccharides (sucrose (table sugar), candy, and soft drinks) cannot be used because the a-glucosidase inhibitory effects delay their hydrolysis and absorption. When used as monotherapy, acarbose and miglitol are not associated with hypoglycemia or significant weight changes. Blocking the absorption of complex carbohydrates decreases the caloric uptake of the small intestine, but the large intestine compensates to assure that adequate caloric goals are met. a-Glucosidase inhibitors do not significantly affect LDL or HDL cholesterol concentrations, but triglyceride levels decline. These agents may prove to be useful in the management of severe hypertriglyceridemia in both the diabetic and non-diabetic population.

General principles of insulin therapy

The goal of insulin replacement therapy is to achieve a blood insulin profile that mimics physiologic insulin secretion. Basal insulin suppresses endogenous glucose production between meals and overnight and boluses of insulin are necessary with meals to promote postprandial glucose utilization. The type, frequency, and timing of insulin injections necessary to achieve this is greatly influenced by the amount of residual b-cell function and concurrent use of oral hypoglycemic agents.

Side effects of insulin

The most significant adverse effect of insulin therapy is hypoglycemia. This is especially the case for treatment of T1DM, but is also true for T2DM. Insulin allergy and lipoatrophy were commonly seen with the use of animal insulin before 'pure' and biosynthetic preparations became available. Both reactions are now rare, but can be seen, probably because there is some degradation during storage and or with depot injection into tissues that can induce an immune response. Weight gain commonly occurs following improved glycemic control with insulin therapy. In the UKPDS, individuals receiving insulin therapy had an average weight gain of 4.0 kg over the course of the study.81

Amylin Analogs Pramlintide

Pramlintide is the first amylin analog commercially available and received FDA approval in March 2005 for therapy in both T1DM and T2DM. Pramlintide, studied as an adjunctive therapy to insulin, has been shown to improve postprandial and overall glycemic control in individuals with both T1DM and T2DM (improvements in HbA1C of 0.67 82 and HbA1C of 0.62 ,83 respectively) without increasing the incidence of hypoglycemia or weight gain. The glycemic improvements with pramlintide had no significant effects on lipid concentrations or blood pressure and showed no evidence of cardiac, hepatic, or renal toxicity. The most frequent adverse side effects associated with pramlintide therapy include transient mild to moderate nausea and anorexia. In its current formulation, pramlintide is administered via subcutaneous injection separately from insulin.

Glucagon Like Peptide1 GLP1 Agonists Exenatide

Glucagon-like peptide-1 (GLP-1) is a 30 31 amino acid peptide released from the distal small bowel and colon and undergoes rapid inactivation by dipeptidyl peptidase-IV (DPP-IV). GLP-1, with a half-life of approximately 90s, augments glucose-mediated b-cell insulin secretion, inhibits glucagon secretion, promotes b-cell proliferation (in animal models), and slows gastric emptying. Augmentation of insulin secretion by GLP-1 is dependent on glucose concentration, and therefore rarely contributes to hypoglycemia when used as monotherapy. Clinically, endogenous levels of GLP-1 are significantly reduced in individuals with T2DM. In clinical trials, exenatide improved postprandial and overall glycemic control in patients with T2DM on metformin monotherapy (decrease in HbA1C of 0.78 ) and was associated with a modest weight loss (mean 2.8 kg) without increasing the incidence of hypoglycemia.84 Similar improvements in glycemic control and sustained weight reduction Adverse events of exenatide...

Dementia Due to Other General Medical Conditions

Dementia also may be caused by other diseases with primarily central nervous system pathology, such as multiple sclerosis, amyotrophic lateral sclerosis, and various conditions (e.g., progressive subcortical gliosis, focal lobar atrophy) with mainly frontal lobe-type behavioral manifestations. Extracerebral pathology, both intracranial (brain tumor, subdural hematoma, hydrocephalus) and extracranial (hypothyroidism, hypercalcemia, hypoglycemia) processes, also can cause dementia via mechanical and biochemical effects on brain function. Accurate diagnosis usually depends on recognition of the characteristic clinical and laboratory features of the underlying illness. The battery suggested in Table 5-4 in Chapter 5 (Dementia and Alzheimer's Disease) is designed to have relatively high sensitivity for this purpose.

Polyglucosan Diseases

A newborn boy was severely jaundiced, and his feeding was difficult because of frequent vomiting. In early childhood, his development was very slow and, after a few years, became arrested. At 7 years of age, he was physically underdeveloped and severely mentally retarded. Bilateral cataracts were diagnosed a few years later. He suffered from hypoglycemic episodes, frequent convulsions, and status epilepticus. Galactosemia. A newborn boy was severely jaundiced, and his feeding was difficult because of frequent vomiting. In early childhood, his development was very slow and, after a few years, became arrested. At 7 years of age, he was physically underdeveloped and severely mentally retarded. Bilateral cataracts were diagnosed a few years later. He suffered from hypoglycemic episodes, frequent convulsions, and status epilepticus.

Toxic Volatile Alcohols

Toxicity CNS > gastrointestinal > metabolic CNS Inebriation, disinhibition, incoordination, blurred vision, diplopia, confusion, CNS and respiratory depression. Gastrointestinal Nausea, vomiting, cramping abdominal pain, gastric bleeding. Metabolic High-anion gap metabolic acidosis, hypoglycemia, hypokalemia, hypomagnesemia, hypophosphatemia, hyperamylasemia.

Nutrition and Epilepsy

Nutrition plays a central role in health and disease processes. The body draws all of its resources except oxygen from the diet. What we consume and how much we consume determines these resources and can influence health and disease. The traditional balanced diet recommended by the American Dietetic Association (ADA) consists of a mixture high in carbohydrates, moderate in protein, and low in fats. Some researchers are criticizing this once accepted food pyramid model that was the framework for a healthy diet for nearly 30 years. Studies on the Atkins diet, a high protein, low carbohydrate diet, support its utility as an effective means for weight loss, but no evidence relates its effects on seizures or long-term safety (1). The ketogenic diet, which is high fat and extremely low in carbohydrates, can help control seizures in some patients (see Chapter 21). Fasting rarely provokes seizures, and actually may reduce seizure frequency by putting the body in a state of ketosis (2,3)....

Uremic Encephalopathy

A 68-year-old diabetic man, following administration of 11 units regular insulin, suffered a hypoglycemic episode with a blood glucose concentration of 28 mg 100 mL for approximately 8 hours. During this episode, he became comatose and, without regaining consciousness, died 15 days later. Eosinophilic neurons and mild astrocytosis (HE) are present in the thalamus.

CASE 3 Changing Insulin Regimen Case Description

Three years and 11 mo following the diagnosis of type 1 diabetes mellitus, he was enrolled in the Diabetes Control and Complications Trial (DCCT). In the DCCT, he was randomized to the experimental arm of the trial that included beginning an intensive insulin regimen of three shots of regular insulin and one shot of ultralente each day. (multiple daily injection MDI program). At entry into the DCCT (March 1987), his hemoglobin A1c (HbA1c) was 7.8 (normal range 4.0-6.3 ). Despite randomization to the intensive insulin regimen, his HbA1c at the time of completion of the trial was 8.3 . The lowest HbA1c achieved during the trial was 7.2 . The patient was quite compliant with the intensive therapy. He experienced hypoglycemia usually two times per week. Despite the study and intervention, his HbA1c did not improve.

Micronutrients Diabetes

Can enhance insulin sensitivity and reduce needs for oral hypoglycemics and or insulin.5-7 Reduces platelet aggregation and risk of thrombosis As a component of GTF, helps control blood glucose and decrease need for insulin or hypoglycemic drugs.1-3 Can be taken together with 5-10 g brewer's yeast

Delirium Due to a General Medical Condition

Metabolic and Endocrine Disturbances. Metabolic causes of delirium include hypoglycemia, electrolyte disturbances, and vitamin deficiency states. The most common endocrine causes are hyperfunction and hypofunction of the thyroid, adrenal, pancreas, pituitary, and parathyroid. Metabolic causes may involve consequences of diseases of particular organs, such as hepatic encephalopathy resulting from liver disease, ure-mic encephalopathy and postdialysis delirium resulting from kidney dysfunction, and carbon dioxide macrosis and hypoxia resulting from lung disease. The metabolic disturbance or endocrinopathy must be known to induce changes in mental status and must be confirmed by lab

Amino And Organic Acid Disorders

Disorders of amino acid or organic acid metabolism are very rare. They typically involve an inherited deficiency or altered function of an enzyme or transport system that mediates the disposition of a particular amino or organic acid (Table 2). The oxidation of amino acids gives rise to ammonia, which is neurotoxic in high concentrations (50). Because the urea cycle functions in the disposal of ammonia, congenital deficiencies of the urea cycle cause hyperammonemia or elevated plasma glutamine (formed from ammonia Fig. 13). The urea cycle defects include carbamyl phosphate synthetase deficiency, or-nithine transcarbamylase deficiency citrullinemia, and argininosuccinic aciduria. The severity of presentation is determined by the particular amino or organic acid abnormality, the duration of the accumulation, and the presence of other metabolic alterations (e.g., hypoglycemia). Dysmyelination, neuronal degeneration, and reactive gliosis are common in patients who die in the first few...

Medical Examination Under Section 4 of the RTA

Whether the examination is carried out by a forensic physician in London or an emergency room physician in San Francisco, the aim of the examination is to exclude any medical condition other than alcohol or drugs as the cause of the driver's behavior. The differential diagnosis is wide and includes head injury, neurological problems (e.g., epilepsy, stroke, cerebral tumour, and multiple sclerosis), metabolic problems (e.g., hypoglycemia), hepatic or renal failure, and mental illness. The procedure should include introductory details, full medical history, and clinical examination. In Scotland, forensic physicians use form F97. Appendix 6 contains a form that has been found useful. Similar forms are not available in the United States, but there is nothing to prevent any emergency department in the United States from drafting and providing a similar document. Even if no special form is provided, most of the relevant material will have been (or at least should be) recorded in the...

Clinical Manifestations Adults And Children

Acute malaria manifests during the erythrocytic phase of infection. Symptoms in immunologically naive hosts are initially nonspecific and include fevers, rigors, headache, myalgias, lethargy, abdominal pain, and vomiting. In children, symptoms may present acutely and in a rapidly progressive fashion with seizures, hypoglycemia, severe anemia, and hypotension. The physical examination may reveal hepatospleno-megaly, but despite hemolysis, jaundice is not frequently observed. Cerebral malaria, characterized by unarousable coma caused by sludging of parasitized erythrocytes in cerebral capillaries, is a severe complication of falciparum malaria and is fatal if untreated.

Challenging Cases in Endocrinology

In medicine, the difficult cases can yield valuable insights because they force physicians to think a little harder when making a diagnosis and to be creative when treating the patient. In Challenging Cases in Endocrinology, distinguished clinician-scientists describe in concise studies their most difficult cases and reveal what they did, how they did it, and why. The cases cover a wide range of medical problems, including pituitary and thyroid tumors, hypopituitarism, hyper- and hypothyroidism, metabolic bone disease, Cushing's syndrome, adrenal insufficiency and cancer, diabetes, and hypoglycemia. Other cases involve disorders of female reproduction, of water balance and lipoprotein metabolism, of puberty, and of growth and development. Each case study reviews how the patient was managed, details the reasons why various tests and treatments many only recently available were carried out, and provides references to ensure that these novel methodologies can be easily translated into...

Of Stress And Glucocorticoids

Inhibition of transporter expression. In addition, short-term exposure to glucocorticoid induces a translocation of the glucose transporter from the cell membrane to intracellular sites in adipocytes via a posttranscriptional mechanism (28). Although these effects of glucocorticoids have been demonstrated in peripheral tissues, it is possible that they have similar actions in brain. Evidence for this hypothesis comes from reports demonstrating that glucocor-ticoids regulate glucose utilization in the brain (29) and decrease glucose uptake in primary neuronal cultures (30,31). This reduction in energy capacity is likely to increase the vulnerability of neurons to other types of insults, such as excitotoxins, hypoxia-ischemia, and hypoglycemia. In addition, over extended periods of time, a reduction in glucose could eventually lead to neurotoxic effects. This possibility is supported by studies of Sapolsky and colleagues on neuronal endangerment, as well as studies from others on the...

Neovastat Ae941 structure unknown

A US open-label, multicenter phase I II study suggested that Neovastat was efficacious in the treatment of refractory metastatic lung cancer 215,302,303 . The study did not demonstrate any serious adverse events. Analysis of data from a group of 48 patients with unresectable late-stage NSCLC from phase I II dose-tolerance trial showed that those receiving more than 2.6 mg kg day Neovastat were 50 less likely to die than those who received less than 2.6 mg kg day 302,304 . Neovastat has now been monitored in over 800 patients, some ofwhom have taken the drug for over 4 years. Overall, Neovastat has an excellent safety profile with few side effects. Although one serious adverse event (hypoglycemia) was noted in type II diabetic patients, other grade III to IV toxicities have not been observed. Phase I II trial of Neovastat (30-240 mL day) conducted in 331 solid-tumor patients demonstrated the most frequent adverse events of nausea (7 ), vomiting (3 ), dyspepsia (2 ) and anorexia (2 )...

Differential Diagnosis

It is important to exclude any potentially treatable causes such as infections with HIV becoming increasingly important. Rarer examples are Whipple's disease, chronic bacterial meningitis, Lyme disease, neurosyphilis and a number of viral encaphalitides (herpes simplex, subacute sclerosing panencephalitis (SSPE), progressive rubella panencephalitis, progressive multifocal leukoencephalopathy). Dementia is also a feature in patients with multiple sclerosis, brain tumor, paraneoplastic disease and metabolic disorders (deficit of vitamin Bi2 or nicotinic acid, hypothyroidism, chronic hypoglycemia, hypo- and hypercalcemia, Cushing's syndrome, Addison's disease, renal impairment leading to uremic encephalopathy and hepatic disturbances). Further, a number of inherited metabolic diseases are associated with cognitive problems (Wilson's disease, metachromatic leukodystrophy, adrenoleukodystrophy, neuronal ceroid-lipofuscinosis, membranous lipodystrophy, Gaucher's disease, Niemann-Pick...

Glitinides nonsulfonylurea secretagogues

The clinical efficacy of glitinides is similar to that of the sulfonylureas. In short-term, placebo-controlled trials, repaglinide monotherapy reduced HbA1C levels from 8.5 at baseline to 7.8 after only 12 weeks. In individuals with T2DM not previously treated with other oral hypoglycemic agents, repaglinide resulted in a 30 decrease in HbA1C, from 6.9 to 4.8 , with fasting and postprandial blood glucose levels decreased by 70 and 112 mgdL_ 1, respectively. Repaglinide59 and nateglinide60 as combination therapy with metformin are more effective than either agent alone. Glitinides are taken before every meal but are not taken if a meal is skipped. As with other insulin secretagogues, hypoglycemia can occur with administration of repaglinide and nateglinide. Due to the short half-life of these drugs hypoglycemia is usually postprandial and of short duration. Repaglinide and nateglinide are both metabolized in the liver and serum drug concentrations may rise in individuals with hepatic...

Definitions

We have defined hypoglycaemia by translating it as 'low blood glucose concentration'. Clinically, episodes of hypoglycaemia are defined as either mild or severe. In mild hypoglycaemia the person experiencing the hypoglycaemia is subjectively aware (symptomatic) of the falling blood glucose concentration at a time when cortical function is sufficiently preserved for the person to recognise the situation and take appropriate action to restore their blood glucose by ingesting carbohydrate. Some authorities also describe a moderate form of hypoglycaemia in which such a symptomatic episode causes significant social disruption. Severe hypoglycaemia is defined as that in which the person experiencing it is too disabled to self-treat and has to be rescued by another person. Again, some authorities add a subdivision of severe hypoglycaemia in which either coma seizure occurs or in which parenteral therapy has to be administered (DCCT 1991).

Toxic Alcohols

Pathway 3 hepatic peroxidase-catalase. Toxicity CNS > gastrointestinal > metabolic. CNS Inebriation, disinhibition, incoordination, blurred vision, diplopia, confusion, CNS and respiratory depression. Gastrointestinal Nausea, vomiting, cramping abdominal pain, gastric bleeding. Metabolic High anion gap metabolic aci-dosis, high osmolal gap metabolic acidosis, hypoglycemia, hypokalemia, hypomagnese-mia, hypophosphatemia, hyperamylasemia.

Chloramphenicol

Cardiovascular (1) Acute cardiovascular collapse in overdose. Treatment orogastric lavage, activated charcoal, exchange transfusion in neonates. (2) Gray baby syndrome hypotension, gray color, vomiting, respiratory distress, hypoglycemia all due to low hepatic conjugation and reduced renal ability to excrete free drug. Hematological Dose-dependent bone marrow (BM) suppression and potentially fatal aplastic anemia.

Epidemiology

Accidental insulin overdose Most common cause of hypoglycemia due to combinations of insulin dose miscalculations, reduced caloric intake, increased exercise level or intercurrent infections or other illnesses. Long-acting (LA) sulfonylureas Most common cause of non-insulin, drug-induced hypoglyce-mia, especially chlorpropamide LA and glybu-ride LA.

Diabetes

Oral hypoglycemics and insulin should be continued and consideration given to supervision of insulin injections. Regular meals and snacks should be provided, and all patients with diabetes should have access to rapidly absorbed, carbohydrate-rich food. Hypoglycemia is easily treated. If the blood glucose is less than 4 mmol L in a conscious person, oral carbohydrates should be given. In a detainee who is

Diabetes Mellitus

Although confusion is a prominent feature in patients who are slipping into hyperglycemic coma, this condition is rarely seen in police custody. Questions relating to fitness for interview and the potential reliability of a detainee's confession are more likely to involve those with hypoglycemia. Episodes of hypoglycemia are associated with irritability, anxiety, and panic in the early stages. As the episode develops, the individual becomes disinhibited and may exhibit childish or aggressive behavior that often mimics drunkenness. Disorientation and mental confusion are common and, in severe cases, the person may pass into a coma. Anybody suffering from hypoglyce-mia will prove to be a poor witness to events that occur during the episode. Most will have complete amnesia for the content of the attack and occasionally for an additional period before the attack occurred when their behavior will have appeared to be normal (96). The doctor should take a clear history of any hypoglycemic...

Sulfonylureas

For nearly 50 years, sulfonylureas, derived from sulfonic acid and urea, have had a central role in oral hypoglycemic therapy of T2DM. Sulfonylureas increase endogenous insulin secretion and can only be used in individuals that have retained significant b-cell function. The combination of efficacy, low incidence of adverse events, and low cost has contributed to their success and continued use. Sulfonylureas are generally safe and are relatively inexpensive. Hypoglycemia is the most common adverse event that is encountered with their use. First-generation Hypoglycemia Weight gain

Galactosemia

The disease presents soon after birth with prolonged jaundice, vomiting, diarrhea, hepatomegaly, and anemia. Untreated patients develop ocular, neurologic, visceral, and metabolic disorders hepatomegaly progressing to nodular cirrhosis kidney dysfunction hypoglycemic episodes and lenticular cataract. Mental retardation, seizures, extrapyramidal and cerebellar symptoms, and

Carnitine

Dairy products the body produces the rest. Patients who are treated with valproic acid can develop carnitine deficiency (32,33). Clinically significant carnitine deficiency is uncommon, however. The most serious problems occur rarely in children (and extremely rarely in adults) with inborn errors of carnitine metabolism that make them especially susceptible to the effects of valproate (34). Possible symptoms of carnitine deficiency include fatigue, muscle weakness, enlarged heart, irregular heartbeat, frequent infection, seizures, poor muscle tone, slow growth, chronic vomiting, chronic fever, hyperammonemia, and hypoglycemia. Carnitine does pass through the blood-brain barrier. Van Wouwe, in his 1995 article, recommends that carnitine deficiency during valproic acid therapy can be reversed within a week by supplementation at 15 mg kg body weight (33).

Diet Memory

Rosclerosis of the cerebral arteries that gradually reduce flow of nutrients and oxygen.9 Foods high in antioxidant nutrients (see pp.115) may reduce free-radical damage to brain cells and reduce risk of atheroscle-rosis.10 In older people decreased digestive function leads to poor absorption of certain nutrients from the diet. Even marginal deficiencies of several of the B vitamins - particularly thiamin, niacin, folate, and vitamin B12 -can impair mental function.911 Reactive hypoglycemia (see pp. 185), triggered by high intakes of refined carbohydrate and sugar, can also interfere with brain function. Brain levels of acetylcholine, a neurotransmitter that is vital to memory, can be maintained by regular consumption of choline-rich foods, such as eggs, nuts, and cauliflower. Over time, regular consumption of a nutritious, well-balanced diet - low in saturated fat, alcohol, and salt, and rich in choline, antioxidant nutrients, minerals, and B vitamins - can help maintain optimum...

Diet Anxiety

In people susceptible to reactive hypoglycemia (see pp. 185), consumption of refined carbohydrates or sugar may trigger increased anxiety and, in rare cases, panic attacks.1 In individuals prone to nervousness and anxiety, consumption of caffeine can worsen their symptoms.2

Diet Stress

Many people make the mistake of relying on large amounts of sugar and coffee during times of stress. Although they may supply short bursts of energy, too much caffeine and refined carbohydrate ultimately worsens chronic fatigue and produces headaches, irritability, and concentration difficulties. Because control of blood glucose is more difficult during times of stress, it is important to minimize intake of refined carbohydrates, which may trigger periods of reactive hypoglycemia (see pp. 185).

Diet Alcohol

Further lowers nutrient absorption from foods. The liver is particularly vulnerable to alcohol - more than three drinks a day causes inflammation and accumulation of fat in the liver. This impairs liver function, reducing the ability to detoxify chemicals and drugs. Because the liver is important for blood sugar control, alcohol-induced liver damage can produce hypoglycemia, leading to fatigue, irritability, and concentration difficulties. Alcohol increases urinary losses of many minerals, including zinc, calcium, and magne-sium.5 Because of these effects, a diet rich in fresh fruits and vegetables, whole grains, lean meats, and low-fat milk products should be carefully chosen.

Biguanides

The specific mechanisms of action of metformin have not been definitively demonstrated. In the liver, metformin increases insulin-dependent suppression of gluconeogenesis and decreases the glucagon-dependent stimulation of gluconeogenesis, resulting in an overall decrease in hepatic glucose production. Animal models suggest additional mechanisms of action for metformin, including insulin-dependent glucose uptake by muscle61 and adipose tissue,62 with resultant increases in glycogen formation, glucose oxidation, and lipogenesis. De Fronzo et al.63 demonstrated that, in humans, improvement in fasting blood glucose on metformin results from reduction in basal hepatic glucose production. In studies using the glucose insulin clamp techniques metformin did not improve whole-body insulin sensitivity in individuals with T2DM. Since the glucose-lowering effect of metformin occurs without stimulation of insulin secretion, metformin is not associated with hypoglycemia when used as monotherapy....

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