Latest Treatment 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, -blockers, chloramphenicol, diso-pyramide, MAOIs, quinine-quinidine, salicy-lates, sulfonamides).
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.
The effect of oral hypoglycemic agents on endothelial function is controversial and probably relates to the agent and model of diabetes being evaluated. Metformin has been shown to improve endothelium-dependent function in the mesenteric arteries of insulin-resistant rats in vitro (165), and the ATP-dependent potassium channel blocker gliclazide ameliorated endothelium-dependent relaxation of the aortas of (alloxan-induced) diabetic rabbits (166). However, clinical studies evaluating the effect of oral hypoglycemics on endothelial function have shown either no difference (167) or diminished reactivity to acetylcholine once the agent is discontinued (120).
Surgical intervention is needed for specific injuries to organs. Diaphragmatic tears are repaired surgically to prevent visceral herniation in later years. Esophageal injury is often managed with gastric decompression with a nasogastric tube, antibiotic therapy, and surgical repair of the esophageal tear. Gastric injury is managed similarly to esophageal injury, although a partial gastrectomy may be needed if extensive injury has occurred. Liver injury may be managed nonoperatively or operatively, depending on the degree of injury and the amount of bleeding. Patients with liver injury are apt to experience problems with albumin formation, serum glucose levels (hypoglycemia in particular), blood coagulation, resistance to infection, and nutritional balance. Management of injuries to the spleen depends on the patient's age, stability, associated injuries, and type of splenic injury. Because removal of the spleen places the patient at risk for immune compromise, splenectomy is...
Beta-adrenergic blocking agents l Hypoglycemic effect also, symptoms of hypoglycemia may be masked Fluconazole T Hypoglycemic effect Histamine H2 antagonists T Hypoglycemic effect due to i breakdown by liver Magnesium salts T Hypoglycemic effect MAO inhibitors T Hypoglycemic effect due to i breakdown by liver Miconazole T Effect of oral hypo-glycemics NSAIDs T Hypoglycemic effect of oral antidiabetics Phenylbutazone T Effect of oral hypoglycemics due to i breakdown by liver, i plasma protein binding, and i renal excretion Probenecid T Hypoglycemic effect Salicylates T Effect of oral hypo-glycemics by i plasma protein binding
Cyclophosphamide (antineoplastic) cyclosporine (immunosuppressant) Cytovene (antiviral drug) Cytoxan (antineoplastic) Cytoxan (antineoplastic) Dantrium (skeletal muscle relaxant) Darvocet-N (analgesic) daunorubicin (antineoplastic) desipramine (antidepressant) DiaBeta (oral hypoglycemic) digitoxin (cardiac glycoside) diphenhydramine (antihistamine) dopamine (sympathomimetic) Edecrin (diuretic) enalapril (ACE inhibitor) enalapril (ACE inhibitor) Eryc (erythromycin base) etidronate (bone growth regulator) etomidate (general anesthetic) Fioricet (analgesic) flurbiprofen (NSAID) folinic acid (leucovorin calcium) Gantrisin (sulfonamide) glipizide (oral hypoglycemic) glyburide (oral hypoglycemic) Hycodan (cough preparation) hydralazine (antihypertensive) hydrocodone (narcotic analgesic) hydromorphone (narcotic analgesic) Hydropres (antihypertensive) Hytone (topical corticosteroid) imipramine (antidepressant) Inderal (beta-adrenergic blocker) Inderal (beta-adrenergic blocker) Indocin (NSAID)...
For more than two decades evidence has been accumulating regarding the hypoglycemic action of soluble fiber. Jenkins et al. (10) reported that the addition of soluble fiber to a test meal lowered blood glucose and insulin response. Kiehm et al. (11) make a similar observation soluble fibers such as guar or pectin were effective (12) but insoluble fibers such as cellulose or wheat bran were not (13). The soluble fibers increased viscosity of the food bolus and it was thought that this reduced the rate of gastric emptying (14). Wolever (15) has reviewed the role of dietary fiber in the management of diabetes fasting serum glucose is reduced, on average, by 16 and plasma cholesterol and triglycerides by 18 and 10 respectively.
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...
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.
Figure 15 Structure of the cofactor undine5diphosphoaDglucuronic 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).
When assessing vital signs, you may note hypertension, a common complication in diabetic patients. Palpate the peripheral pulses to determine their strength, regularity, and symmetry. During the neurological examination, use an ophthalmoscope to evaluate the patient for retinopathy or cataracts. Assess the patient for any signs and symptoms of hypoglycemia or hyperglycemia (Table 2).
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.
High anaphylaxis risk Nonselectives block cat-echol'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.
Consideration of the derangements in platelet function, the coagulation system, and the fibrinolytic system and their contributions to exacerbation of macrovascular disease in type 2 diabetes gives rise to several therapeutic approaches. Empirical use of aspirin (160-325 mg per day in a single dose) seems appropriate in view of the high likelihood that covert CAD is present even in asymptomatic people with type 2 diabetes and the compelling evidence that prophylactic aspirin reduces the risk of heart attack when CAD is extant. Because many of the derangements contributing to a prothrombotic state in diabetes are caused by hyperglycemia, rigorous glycemic control is essential. Accordingly, the use of diet, exercise, oral hypoglycemic agents, insulin sensitizers, and if necessary insulin itself is appropriate to lower HbA1c to 7 . Because other derangements contributing to a prothrombotic state such as attenuation of fibrinolysis appear to be related to insulin resistance and...
Naturally, another question arises how low should the blood sugar level be Is a very low concentration actually dangerous In the patients treated intensively with insulin, there was a risk of hypoglycaemia (dangerously low blood sugar). In the DCCT, particular attention was paid to the 'danger' of intensive therapy. Patients undergoing such therapy did in fact experience hypogly-caemia more frequently than those treated conventionally. Considering the poor metabolic control observed in the conventionally treated group, this is hardly surprising.
Cerebral dysfunction occurs when the central nervous system (CNS) is deprived of glucose for cellular needs. In contrast to muscle and fat cells in the body that can break down amino and fatty acids for energy, the brain cells depend on glucose for energy. When the liver's supply of glycogen is depleted and no replacement is available, brain damage results. Prolonged periods of hypoglycemia can lead to coma, permanent brain damage, and death.
Treats hypoglycemia if the person cannot maintain oral intake and if IV access is not available note that the drug may cause vomiting Teach the patient and family prevention, detection, and treatment of hypoglycemia. Encourage a daily exercise, diet, and medication regimen on a consistent basis. Remind the patient to consume extra foods before increased exercise and to carry a rapid-absorbing carbohydrate at all times. Teach the patient and significant others to keep glucagon available in the home or at work or school. Instruct coworkers, teachers, and neighbors how to treat hypoglycemia. Physical response Patency of airway, regularity of breathing, adequacy of circulation assessment of the CNS (level of consciousness, signs and symptoms of hypoglycemia strength and motion of extremities pupillary response SNS response) response to therapeutic interventions Teach the patient and significant others about the signs and symptoms of hypoglycemia and how to manage them at home. Include the...
Pentamidine is an alternative in patients who have adverse reactions or fail to respond to TMP-SMX. The dosage is 4 mg kg day IV for 14-21 days. Adverse effects include anemia (33 ), creatinine elevation (60 ), LFT elevation (63 ), and hyponatremia (56 ). Pancreatitis, hypo-glycemia, and hyperglycemia are common side effects.
In Madagascar the plant is widespread, reflecting its multiple uses in herbal treatments. The striking floral display of the plant has promoted its spread around the world and has led to variations in its medicinal applications. By the early 20th century it was being used as an oral hypoglycemic agent (to lower blood sugar levels) in South Africa, southern Europe, and the Philippines to treat diabetic ulcers in the West Indies and to control hemorrhages and scurvy in Brazil. The role
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.
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
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 P-cell insulin secretion, inhibits glucagon secretion, promotes P-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...
While most homicidal suffocation of infants is sporadic, a small number of individuals, virtually all of whom are mothers, practice a lethal form of Munchausen's syndrome by proxy, a form of child abuse in which children are brought to physicians and hospitals for induced signs and symptoms of illnesses in conjunction with a fictitious history.14 The child is usually subjected to multiple hospital admissions and extensive medical evaluations, treatments and procedures for these nonexistent medical conditions. Thus, a child might be brought into the hospital with hypoglycemia because the mother is administering insulin or there may be blood in the urine because the mother pricks her own finger and adds blood to the child's urine.
Action Kinetics Concentrated insulin injection (500 U mL). Depending on response, may be given SC or IM as a single or as two or three divided doses. Not suitable for IV administration because of possible allergic or anaphylactoid reactions. Uses Insulin resistance requiring more than 200 units insulin day. Contraindications Allergy to pork or mixed pork beef insulin (unless client has been desensitized). Special Concerns Use with caution during lactation. Additional Side Effects Deep secondary hypoglycemia 18 24 hr after administration. Drug Interactions Do not use together with PO hypoglycemic agents.
Hepatic encephalopathy is a diagnosis of exclusion. Therefore, if a patient with acute or chronic liver failure suddenly develops altered mental status, concomitant problems must be excluded, such as intracranial lesions (hemorrhage, infarct, tumor, abscess), infections (meningitis, encephalitis, sepsis), metabolic encephalopathies (hyperglycemia or hypoglycemia, uremia, electrolyte imbalance), alcohol intoxication or withdrawal, Wernicke's encephalopathy, drug toxicity (sedatives, psycho-active medications), or postictal encephalopathy.
Two methods of insulin therapy are described daily subcutaneous injections of insulin for short-term maintenance and subcutaneous implantation of timed-release pellets of bovine insulin for long-term maintenance. The goal of treatment is not to produce a normal blood glucose concentration, as such tight control poses the risk of death from hypoglycemia, but rather to maintain growth and prevent ketoacidosis for the duration of the experiment. The dose of insulin is chosen on this basis. It is not necessary to monitor blood glucose concentrations in treated animals unless this parameter is a variable in an experimental study.
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.
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.
Hyperviscosity in this disease is directly related to neurologic impairment in the neonate. It is important to note that the peripheral hematocrit is disproportionate to the central nervous system hematocrit and should not be used as a guideline to estimate the degree of viscosity. Decision is based on both clinical and metabolic status, lethargy, hypoglycemia, and hypocalcemia.
Therapeutic objectives are (1) prevention of life-threatening hypergly-cemic (diabetic) coma (2) prevention of diabetic sequelae (angiopathy with blindness, myocardial infarction, renal failure), with precise titration of the patient being essential to avoid even short-term spells of pathological hyperglycemia (3) prevention of insulin overdosage leading to life-threatening hypoglycemic shock (CNS disturbance due to lack of glucose). Any change in eating and living habits can upset control of blood sugar skipping a meal or unusual physical stress leads to hypoglycemia increased CH intake provokes hyperglycemia. Hypoglycemia is heralded by warning signs tachycardia, unrest, tremor, pallor, profuse sweating. Some of these are due to the release of glucose-mobilizing epinephrine. Counter-measures glucose administration, rapidly absorbed CH orally or 10-20 g glucose i.v. in case of unconsciousness if necessary, injection of glucagon, the pancreatic hyperglycemic hormone.
A database with compounds in seven different pharmacological classes of activity was used for development of discriminant models of each activity class. The classes included analgesic, antiviral, bronchodilator, antifungal, hypolipidemic, hypoglycemic, and beta-blocking activity. Galvez developed separate discriminant models for each class by using molecular connectivity indices. Based on each model, activity was predicted for a list of structures as both a prediction and a subsequent experimental test. In some cases, compounds were also tested experimentally. Compounds predicted to be active were generally known from the literature to be active or tested in the laboratory.
Special Concerns Cardiovascular collapse, acute CHF, acute MI, and other conditions characterized by hypoxia have been associated with lactic acidosis, which may also be caused by metformin. Use of oral hypoglycemic agents may increase the risk of cardiovascular mortality. Although hypoglycemia does not usually occur with metformin, it may result with deficient caloric intake, with strenuous exercise not supplemented by increased intake of calories, or when metformin is taken with sulfonylureas or alcohol. Because of age-related decreases in renal function, use with caution as age increases. Safety and efficacy have not been determined in children. Side Effects Metabolic Lactic acidosis (fatal in approximately 50 of cases). Oral Unpleasant or metallic taste. GI Diarrhea, N&V, abdominal bloating, flatulence, anorexia. He-matologic Asymptomatic subnormal serum vitamin B12 levels. Drug Interactions None reported that would interact with dental therapy or oral health. How Supplied Tablet...
Insulin glargine (Lantus) contains two modifications of the human insulin molecule that change both the onset and duration of action. Two arginine residues are added to the carboxyl terminal end of the insulin B-chain, and glycine is substituted for asparagine at the end of the A-chain (position A21). The latter modification prevents deamidation and dimerization. Overall, these changes result in a stable molecule that is soluble at an acidic pH but insoluble at the neutral pH of subcutaneous tissues. When insulin glargine is injected subcutaneously, the acidic solution is neutralized. Microprecipitates of insulin glargine form in the subcutaneous tissue and are slowly absorbed over a period of up to 24 h, resulting in a nearly constant level of insulin throughout the day. Insulin glargine may be given at any time of day and has been shown to cause less nocturnal hypoglycemia when used at bedtime than NPH insulin. Insulin glargine cannot be mixed prior to injection with any other...
Human recombinant DNA produced regular insulin has an onset of action between 30 and 60 min after and a peak effect 2-4 h after injection, with a usual duration of action of 6-8 h. Regular insulin was the shortest acting insulin available prior to the availability of the rapid-acting analogs. Its duration of action extends beyond the duration of digestion and absorption of most meals, thereby increasing the risk of hypoglycemia.
We can more easily understand the logic of the synergistic interactions of the GR and PPAR RXR signal pathways on mHS gene expression, when we realise that one of the functions of glucocorticoid release into the blood is in the response of starvation stress.21 Starvation partly parallels the situations of the suckling neonate or the adult on a high fat low carbohydrate diet in that all three situations result in elevated plasma free fatty acid concentrations.22,23 In the case of starvation, plasma free fatty acid concentrations increase as a result of fat mobilization from adipose tissue, in an attempt by the body to compensate for low blood glucose fuel availability. Such fatty acids are predictably converted to ketone bodies, via the hepatic HMG-CoA cycle, resulting in a significant hyperketonaemia that can provide up to 70 of the fuel requirements of the brain during starvation.22,23 Glucocorticoids released from the adrenal cortex act to effect such increases in plasma free fatty...
Reinforce the need for small, frequent meals. Warn against overeating at any one meal, which places too great a demand on the pancreas, and stress limiting caffeine and alcohol. Instruct the patient to inspect her or his stools daily and report to the physician any signs of steatorrhea. Teach the patient and family the care related to surgically induced diabetes symptoms and appropriate treatment for hypoglycemia and hyperglycemia, procedure for performing blood glucose monitoring, administration of insulin injections. Teach the patient or significant other to change the dressing over the abdominal incision and empty the drains daily (if present).
The study used the QWB-SA to explore the relationship between measures of glycemia and health-related quality of life. Glycemia was measured with self-reported frequency of symptomatic hypoglycemia and hyperglycemia, and HbA1c. HRQOL and health utility scores were assessed with the QWB-SA.
Poorly controlled gestational diabetes is associated with an increase in the incidence of preeclampsia, polyhydramnios, fetal macrosomia, birth trauma, operative delivery, and neonatal hypoglycemia. There is an increased incidence of hyperbilirubinemia, hypocalcemia, and erythremia. Later development of diabetes mellitus in the mother is also more frequent. The prevalence of gestational diabetes is higher in black, Hispanic, Native American, and Asian women than white women. The prevalence of gestational diabetes is 1.4 to 14 percent.
Patients generally have a rostrocaudal deterioration that is characteristic of supratentorial mass lesions, which does not occur in metabolic brain disease, and the anatomical defect is not regionally restricted as it is with subtentorial damage. The clinical signs are certainly helpful, but there is too much overlap to allow the diagnosis to be established by the clinical findings alone. It is not uncommon, for example, for patients with hepatic encephalopathy or hypoglycemia to develop focal motor signs such as hemiparesis or visual field defects, which are characteristic of a structural lesion, whereas patients with multiple brain metastases may develop nothing other than a global alteration of cognitive function.
Hematologic Agranulocytosis, thrombocytopenia. Allergic Fever, sore throat, respiratory distress, rash, pharyngitis, laryngospasm, anaphylaxis. Skin Fever, pruritus, rash. Ophthalmic Dry eyes. GU Decreased libido, impotence, urinary tract infection. Other Hypoglycemia. Respiratory Bron-chospasm, dyspnea, wheezing. Additional Side Effects Psoriasislike eruptions, skin necrosis, SLE (rare).
Related to (Specify hyperglycemia or hypoglycemia.) Defining Characteristics (Specify hyperglycemia fatigue, irritability, headache, abdominal discomfort, weight loss, polyuria, polydipsia, polyphagia, dehydration, blurred vision hypoglycemia nervousness, sweating, hunger, palpitations, weakness, dizziness, pallor, behavior changes, uncoordinated gait.) Goal Client will not experience injury from hyperglycemia or hypoglycemia. Outcome Criteria Provides insulin replacement to maintain normal blood glucose levels without causing hypoglycemia two or more injections may be given daily SC with a portable syringe pump or by intermittent bolus injections with a syringe and needle. Promote exercise program consistent with dietary and insulin regimen teach to increase carbohydrate intake before vigorous activities. hypoglycemia. Assess for signs and symptoms of hypoglycemia, blood-glucose level. Provide rest and immediate source of a simple carbohydrate such as honey, milk, or fruit juice...
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.
In human patients with SCAD or MCAD deficiency the common features include hypoglycemia, hyperammonemia, metabolic acidosis, organic acidemia and a fatty change of liver.4,15,16,17 As stated previously there are no overt clinical signs reported in these mice however, they do show several biochemical and pathological features. We have found that upon fasting SCAD deficient mice under 8 weeks of age that the blood glucose will drop in half as compared to normal controls.3 In our experience, normal mouse blood glucose concentrations run approximately 150-200 mg dl and the fasted mutants will drop to 70-90 mg dl this is apparently not low enough induce any clinical signs of hypoglycemia. Yamanaka and colleagues have confirmed the hypoglycemia in the mutant mice,19 and studies using perfused liver from these mice also showed glucose production was lower in the mutants, as well as a failure to increase ketone body production using either butyrate, octanoate, or oleate as substrates.19...
As mentioned, human patients with acyl-CoA dehydrogenase deficiencies share the disease features of hypoglycemia, hyperammonemia, tissue fatty change, hypoketonemia, carnitine deficiency and organic acidemia due to apparent disruption of normal fatty acid, glucose and urea metabolism. Most of the acute clinical episodes occur in young children. These episodes are precipitated by fasting and are often fatal with the in vivo mechanisms essentially unknown. Since the genes of the rate controlling enzymes of these pathways are tissue and developmentally regulated at the transcriptional level, we measured, throughout neonatal development, the steady-state mRNA levels of long-chain (LCAD), medium-chain (MCAD), short-chain (SCAD) acyl-CoA dehydrogenases, pyruvate carboxylase (PC), phosphoenolpyruvate carboxykinase (PEPCK), carbamyl phosphate synthetase I (CPS), ornithine transcarbamylase (OTC), and argininosuccinate synthetase (AS) in fed or fasted-SCAD deficient BALB cByJ mice, as compared...
Until the introduction of radioimmunoassay, death caused by insulin was extremely difficult to prove. Most deaths from insulin are accidental. Suicides are infrequent and homicides rare. Insulin, of course, is used for the treatment of diabetes. An overdose of insulin will cause hypoglycemia with irreversible injury to the brain. In one 6-month period, one of the authors (VJMD) saw five deaths caused by insulin a homicide, a suicide, and three accidents. The homicide involved a 43-year-old nondiabetic male who was found dead in bed by his wife. She summoned the police and told them he had been hospitalized for bleeding caused by liver disease, but refused to stay in the hospital. She also told them he had been drinking heavily since he had returned home. A physician at one of the hospitals he had been seen at was contacted and agreed to sign the death certificate. Subsequently, it turned out that this was not the deceased's treating physician. The body was transported to a funeral...
Metformin is an oral hypoglycemic agent that is extensively used for the treatment of type 2 diabetes mellitus. Its mechanism of action involves decreasing hepatic glucogenolysis that leads to a decrease in hepatic glucose output. To a lesser extent metformin increases peripheral glucose-mediated glucose uptake (209).
Insulin-dependent diabetes mellitus (IDDM) is a metabolic disorder caused by a deficiency of insulin. The deficiency is thought to occur in those individuals who are genetically predisposed to the disease and who have experienced a precipitating event, commonly a viral infection or environmental change, that causes an autoimmune condition affecting the beta cells of the pancreas. It is treated by injection of insulin and regulation of diet and activity that maintain body functions. Complications that occur from improper coordination of these include hypoglycemia and hyperglycemia which, if untreated, lead to insulin shock or ketoacidosis. Long-term effects of the disease include neuropathy, nephropathy, retinopathy, atherosclerosis, and microangiopathy.
Contraindications use during episodes of hypoglycemia. Hypersensitiv-ity to insulin lispro. Special Concerns Since insulin lis-pro has a more rapid onset and shorter duration of action than regular insulin, clients with type I diabetes also require a longer acting insulin to maintain glucose control. Requirements may be decreased in impaired renal or hepatic function. use with caution during lactation. Safety and efficacy have not been determined in children less than 12 years of age.
According to Heaton (30), dietary fiber is generally resistant to digestion but its most important characteristic is that it constitutes the physical form and texture of whole foods. This structure affects several physiological phenomena eating time, degree of satiety, rate of digestion, and extent of digestion. The presence of dietary fiber with an intact botanical structure prevents the high insuli-nemic peak following mastication and ingestion of an apple, and it also prevents the resulting hypoglycemia 2h after. The homogenization of the apple in apple puree destroys its botanical structure and largely reduces the beneficial physiological effects of the whole apple, even if its composition is not affected. The food
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...
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 dysfunction. Repaglinide is metabolized by the cytochrome P450 enzyme CYP3A4 and concurrent use with other drugs that induce or suppress this enzyme may alter its glycemic effects.
Approximately 30 of the patients on a general hospital unit are alcohol-dependent however, only 2 of them have a diagnosis of alcohol dependence or alcoholism. The other 28 have been admitted for a variety of reasons. Illnesses such as esophagitis, gastritis, ulcers, hypoglycemia, pancreatitis, and some anemias can be attributed directly to alcohol usage. Chronic alcohol dependence is the most common cause of cardiomyopathy. There is also an increased incidence of injuries, falls, and hip fractures related to high blood alcohol levels.
Contraindications Diabetic ketoa-cidosis, cirrhosis, inflammatory bowel disease, colonic ulceration, partial intestinal obstruction or predisposition to intestinal obstruction, chronic intestinal diseases associated with marked disorders of digestion or absorption, conditions that may deteriorate as a result of increased gas formation in the intestine. In significant renal dysfunction. Severe, persistent bradycardia. Lactation. Special Concerns Safety and efficacy have not been determined in children. Acarbose does not cause hypo-glycemia however, sulfonylureas and insulin can lower blood glucose sufficiently to cause symptoms or even life-threatening hypoglycemia. Side Effects GI Abdominal pain, diarrhea, flatulence. GI side effects may be severe and be confused with paralytic ileus. Drug Interactions Charcoal l Effect of acarbose Digestive enzymes l Effect of acar-bose Digoxin l Serum digoxin levels Insulin T Hypoglycemia which may cause severe hypoglycemia Sulfonylureas T...
Ness, drowsiness, fatigue, hallucinations, insomnia, lethargy, mental changes, memory loss, strange dreams. GI Diarrhea, ischemic colitis, nausea, mesenteric arterial thrombosis, vomiting. Hematologic Agranulocytosis, thrombocytopenia. Allergic Fever, sore throat, respiratory distress, rash, pharyngitis, laryngos-pasm, anaphylaxis. Skin Pruritus, rash, increased skin pigmentation, sweating, dry skin, alopecia, skin irritation, psoriasis. Ophthalmic Dry, burning eyes. GU Dysuria, impotence, nocturia. Other Hypoglycemia or hyperglycemia. Respiratory Bronchospasm, dyspnea, wheezing. Drug Interactions See also Drug Interactions for Beta-Adrenergic Blocking Agents and Antihypertensive Agents.
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.
Reyes syndrome is an entity of unknown etiology affecting children, in which an upper respiratory tract infection, chicken pox, and, rarely, gastroenteritis are followed by vomiting, convulsion, coma, hypoglycemia, elevated blood ammonia, and abnormal serum transaminase values. Individuals dying of the entity show fatty metamorphosis of the liver, with multiple small fatty cyto-plasmic vesicles in the hepatocytes, myocardial fibers, and tubular cells of the kidneys. These are extremely fine vesicles compared with the coarse deposit seen in alcoholic fatty metamorphosis of the liver. Reyes syndrome can be confused with inborn errors of metabolism with which it may share many of the same clinical characteristics. The only way to be absolutely sure of the diagnosis is to demonstrate specific mitochondrial changes in liver tissue.
In a term neonate with a low free T4 but normal TSH level, true central hypothyroidism, which is quite rare, should be ruled out. Mutations in the gene coding for the beta subunit of TSH or the TRH receptor could be the causes 32, 33 . Central hypothyroidism could coincide with other anterior pituitary hormone deficiencies hypoglycemia, microphallus, prolonged jaundice and or cryptorchidism 34-36 .
Both first-generation sulfonylureas (tolbutamide, chlorpropamide, tolazamide, and acetohexamide) and second-generation sulfonylureas (glyburide, glipizide, and glimepiride) are rapidly absorbed after oral administration. The half-lives are between 4 and 10 h with the duration of glycemic effect ranging from 6 to 24 h. The exception is chlorpropamide, which has a half-life of 25-60 h and a duration of glycemic effect of 24-72 h. Most sulfonylureas are hepatically metabolized and renally cleared. Active circulating metabolites may prolong the hypoglycemic effect, especially in individuals with acute or chronic renal impairment.
Sulfonylureas increase endogenous insulin secretion. Their efficacy, measured by the plasma glucose lowering effect, is greatest in individuals with newly diagnosed T2DM. Clinical studies have shown that sulfonylureas reduce mean FPG to 54-72 mgdL_ 1 and HbA1C levels by 1.5-2 . The benefit of sulfonylurea therapy depends on the initial degree of hyperglycemia, duration of diabetes (more effective in T2DM of shorter duration), and previous use of other oral hypoglycemic agents. Because many of the sulfonylurea metabolites are active, more conservative dosing is advised in any patient who may be at high risk for decreased hepatic metabolism or renal clearance of the active drug or metabolites.
The risk of hypoglycemia on metformin monotherapy is extremely low. Combination therapy with other oral hypoglycemic agents increases this risk. Metformin therapy, unlike other oral hypoglycemic agents, is not associated with weight gain but a modest weight loss of 2-3 kg. Long-term therapy with metformin is also associated with decreases in serum concentrations of plasma triglycerides (10-20 reduction), total cholesterol (5-10 reduction), and LDL cholesterol, with some studies noting a slight increase in HDL cholesterol.
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.
Hypoglycemia results from absolute or relative over-dosage (see p. 260). Allergic reactions are rare locally redness at injection site, atrophy of adipose tissue (lipodystro-phy) systemically urticaria, skin rash, anaphylaxis. Insulin resistance can result from binding to inactivating antibodies. A possible local lipohypertrophy can be avoided by alternating injection sites.
Action Kinetics Acts by delaying digestion of ingested carbohydrates resulting in smaller rise in blood glucose levels after meals. Does not enhance insulin secretion or increase insulin sensitivity. Does not cause hypoglycemia when given in fasted state. Absorption is saturable at high doses (i.e., only 50 to 70 of 100 mg dose is absorbed while 25 mg dose is
Type 1 diabetes is defined as the failure of pancreatic b-cells to secret insulin and can be subdivided into type 1A and 1B diabetes. Type 1A results from chronic, progressive T cell-mediated autoimmune destruction of the b-cells of the pancreas, eventually leading to severe insulin deficiency. The rate of b-cell destruction is quite variable, being rapid in some individuals, especially infants and young children, and slower in adolescents and adults. The disease occurs throughout childhood and adolescence in genetically predisposed individuals. Type 1A diabetes predominantly affects European Caucasians and is less frequent in African Americans, Asians, and Native North Americans. Type 1B diabetes has a low prevalence rate with unknown etiology and it is strongly inherited. There is no evidence of b-cell autoimmunity associated with type 1B diabetes. Patients with type 1 diabetes should receive insulin frequently and do not respond well to oral hypoglycemic drugs.13 Type 2 diabetes...
Measurements of blood glucose in women with type 1 diabetes should occur at 7 30 AM, 10 AM, 1 PM, 4 30 PM, and 6 30 PM. If the first morning blood glucose value is high, testing should also be performed at bedtime and in middle of the night. Bedtime and middle-of-the-night tests are important to discover, treat, and prevent nocturnal hypoglycemia.
As the mother enters active labor, insulin resistance rapidly decreases and insulin requirements fall rapidly. Thus, continuing insulin therapy is likely to lead to hypoglycemia. To prevent this, glucose should be infused at a rate of 2.5 mg kg per min. Capillary blood glucose should be measured hourly. The glucose infusion should be doubled for the next hour if the blood glucose value is less than 60 mg dL. On the other hand, values of 120 mg dL or more require the administration of regular insulin subcutaneously or intravenously until the blood glucose value falls to 70 to 90 mg dL. At this time, the insulin dose is titrated to maintain normoglycemia while glucose is infused at a rate of 2.5 mg kg per min.
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
Action Kinetics Effective in some with a history of coma or ketoacido-sis may be effective in clients who do not respond well to other oral antidi-abetics. Use with insulin is not recommended for maintenance. Onset 4-6 hr. tv2 7 hr. Time to peak levels 3-4 hr. Duration 12-24 hr. Metabolized in liver to metabolites with minor hypoglycemic activity. Excreted through the kidneys (85 ) and feces (7 ).
Absent at rest. Mainly PosT.1 Stress (anxiety, fatigue, excitement, cold). Metabolic disturbances (hyperthyroidism, hypoglycemia, pheochromocytoma). Drugs toxins (alcohol or drug withdrawal mercury, manganese, lithium, valproic acid, cyclosporine A, amiodarone, flunarizine, cinnarizine, tricyclic antidepressants, neuroleptics o tardive tremor)
PPARs are also activated by synthetic ligands, some of them being already marketed drugs, such as fibrates, targeting PPARa as hypolipidemic drugs in the preventive treatment of coronary artery disease, and thiazolidinediones, targeting PPARg as hypoglycemic drugs in the treatment of type 2 diabetes. However, due to the pleiotropic effects of PPARs, these drugs present unwanted side effects, such as weight gain and edema in the case of PPARg agonists. Designing selective modulators that could differentially recruit coactivators in order to minimize side effects constitutes a real challenge and an important therapeutic goal. Dual PPARa g agonists and PPAR panagonists are currently being developed to improve the management of type 2 diabetes and dyslipidemia, and for the treatment of the metabolic
As discussed above, the primary disadvantage of sulfonylurea use is a risk of hypoglycemia, especially in individuals with hepatic or renal dysfunction. Drug interactions between sulfonylureas and other pharmacologic agents (salicylates, sulfonamides, fibric acid derivatives, and warfarin) can prolong the activity of either medication, and requires both close glucose monitoring and measurement of serum drug levels when possible. The activity of metabolites prolongs the drug effect, which can be beneficial in improving glycemic control, but dangerous if buildup of the metabolites occurs. Finally, weight gain is common in persons on sulfonylurea therapy.
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