Wednesday, 2 July 2008
Gestational diabetes is a type of diabetes that occurs only during pregnancy.Gestational diabetes starts when the body is not able to make and use all the insulin it needs for pregnancy. Without enough insulin, glucose cannot leave the blood and be changed to energy. Glucose builds up in the blood to high levels.
When the mother who does not have diabetes develops a resistance to insulin because of the hormones pregnancy.women with gestational diabetes may be non-insulin dependent or insulin dependent.
that leads to increased blood sugar levels,happen during the 20th weeks to 24th weeks of prgenancy
Why GDM Occurs?
  • During pregnancy,many physiological changes take place.Changes in metabolism can be seen.
  • Insulin function may not be as effective during pregnancy
  • The palcenta makes certain hormones that may prevent insulin from working the way that it should.
  • The body has to make three times more insulin than normal to offset the hormones made by the pacenta since a growing fetus is dependent on the mother's nutrient supply of glucose,amino acids, and lipids.
  • About 5 % of prgenant women are unable to produce enough insulin
  • When this condition happens,it is referred to as insulin resistance.

With each feeding, the pregnant woman undergoes a complex series of maternal hormonal actions (ie, a rise in blood glucose; the secondary secretion of pancreatic insulin, glucagon, somatomedins, and adrenal catecholamines). These adjustments ensure that an ample, but not excessive, supply of glucose is available to the mother and fetus. The key features of this complex interaction include the following:

  • Compared to nonpregnant subjects, pregnant women tend to develop hypoglycemia (plasma glucose mean = 65-75 mg/dL) between meals and during sleep. This occurs because the fetus continues to draw glucose across the placenta from the maternal bloodstream, even during periods of fasting. Interprandial hypoglycemia becomes increasingly marked as pregnancy progresses and the glucose demand of the fetus increases.
  • Levels of placental steroid and peptide hormones (eg, estrogens, progesterone, and chorionic somatomammotropin) rise linearly throughout the second and third trimesters. Because these hormones confer increasing tissue insulin resistance as their levels rise, the demand for increased insulin secretion with feeding escalates progressively during pregnancy. Twenty-four–hour mean insulin levels are 50% higher in the third trimester compared to the nonpregnant state.
  • If the maternal pancreatic insulin response is inadequate, maternal and, then, fetal hyperglycemia results. This typically manifests as recurrent postprandial hyperglycemic episodes. These postprandial episodes are most significantly accountable for the accelerated growth exhibited by the fetus.
  • Surging maternal and fetal glucose levels are accompanied by episodic fetal hyperinsulinemia. Fetal hyperinsulinemia promotes excess nutrient storage, resulting in macrosomia. The energy expenditure associated with the conversion of excess glucose into fat causes depletion in fetal oxygen levels.
  • These episodes of fetal hypoxia are accompanied by surges in adrenal catecholamines, which, in turn, cause hypertension, cardiac remodeling and hypertrophy, stimulation of erythropoietin, red cell hyperplasia, and increased hematocrit. Polycythemia (hematocrit >65%) occurs in 5-10% of newborns of diabetic mothers. This finding appears to be related to the level of glycemic control and is mediated by decreased fetal oxygen tension. High hematocrit values in the neonate lead to vascular sludging, poor circulation, and postnatal hyperbilirubinemia.

During a healthy pregnancy, mean fasting blood sugar levels decline progressively to a remarkably low value of 74 � 2.7 (SD) mg/dL. On the other hand, peak postprandial blood sugar values rarely exceed 120 mg/dL. Meticulous replication of the normal glycemic profile during pregnancy has been demonstrated to reduce the macrosomia rate. Specifically, when 2 hour postprandial glucose levels are maintained less than 120 mg/dL, approximately 20% of fetuses demonstrate macrosomia. Conversely, if postprandial levels range up to 160 mg/dL, macrosomia rates rise to 35%.

  • Fetal morbidity with diabetes during pregnancy
    • Miscarriages
      • In all women with preexisting diabetes mellitus, there is a 9-14% rate of miscarriage.
      • Current data suggest a strong association between degree of glycemic control prior to pregnancy and miscarriage rate. Suboptimal glycemic control has been shown to double the miscarriage rate in women with diabetes. A correlation also exists between more advanced diabetes and miscarriage rates. Patients with long-standing (>10 y) and poorly controlled (glycohemoglobin exceeding 11%) diabetes have been shown to have a miscarriage rate of up to 44%. Conversely, reports demonstrate a normalization of miscarriage rate with excellent glycemic control.
    • Birth defects
      • Among the general population, major birth defects occur in 1-2% of the population. In women with overt diabetes and suboptimal glycemic control prior to conception, the likelihood of a structural anomaly is increased 4- to 8-fold.
      • Although initial reports demonstrated anomaly rates as high as 18% in women with preexisting diabetes mellitus,more recent reports with more aggressive preconception and first trimester management report anomaly rates between 5.1 and 9.8%.
      • Two-thirds of anomalies involve the cardiovascular and central nervous systems. Neural tube defects occur 13-20 times more frequently in diabetic pregnancy. Genitourinary, gastrointestinal, and skeletal anomalies are also more common.
      • The fact that no increase in birth defects occurs among the offspring of fathers who are diabetic and women who develop gestational diabetes after the first trimester is notable. This suggests that periconceptional glycemic control is the main determinant of abnormal fetal development in diabetic women.
      • When the frequency of congenital anomalies in patients with normal or high first-trimester maternal glycohemoglobin values was compared to the frequency in healthy patients, the rate of anomalies was only 3.4% with glycosylated hemoglobin values (HbA1C) of less than 8.5%, whereas patients with poorer glycemic control in the periconceptional period (HbA1C >8.5%) had a 22.4% rate of malformations. An overall malformation rate of 13.3% was reported in 105 patients with diabetes, but the risk of delivering a malformed infant was comparable to a normal population when the glycosylated hemoglobin (HbA1c ) was less than 7%. More recently, in a review of 7 cohort studies, researchers found that patients with a normal glycohemoglobin (0 SD above normal), the absolute risk of an anomaly was 2%. At 2 SD above normal, this risk was 3%, with an odds ratio of 1.2 (1.1- 1.4). As the glycohemoglobin increased so did the risk for malformation in a direct relationship.
      • Because birth defects occur during the critical 3-6 weeks after conception, nutritional and metabolic intervention must be initiated well before pregnancy begins. Clinical trials of intensive metabolic care have demonstrated that malformation rates similar to those in the nondiabetic population can be achieved with meticulous preconceptional glycemic control. Subsequent trials comparing a preconceptional intensive metabolic program to standard treatment over 15 years duration have demonstrated lowered perinatal mortality (0% vs 7%) and reduced congenital anomaly rate (14% to 2%). In addition, when the preconceptional counseling program was discontinued, the congenital anomaly rate increased by over 50%.
    • Growth restriction
      • Although most fetuses of diabetic mothers exhibit growth acceleration, growth restriction occurs with significant frequency in pregnancies in women with preexisting type 1 diabetes.
      • The most import predictor of fetal growth restriction is underlying maternal vascular disease. Specifically, pregnant patients with diabetes-associated retinal or renal vasculopathies and/or chronic hypertension are most at risk for growth restriction.
    • Growth acceleration
      • Excessive body fat stores, stimulated by excessive glucose delivery during diabetic pregnancy, often extends into childhood and adult life.
      • Approximately 30% of fetuses of women with diabetes mellitus in pregnancy are large for gestational age (LGA). In preexisting diabetes mellitus this incidence appears slightly higher, 38%.
      • Maternal obesity, common in type 2 diabetes, appears to significantly accelerate the risk of infants being LGA.
    • Fetal obesity
      • Macrosomia is typically defined as a birthweight above the 90th percentile for gestational age or greater than 4000 grams. In pregnant diabetic women, macrosomia occurs in 15-45% of cases, a 3-fold increase from normoglycemic controls.
      • Newborns with macrosomia experience excessive rates of neonatal morbidity, as illustrated by a study by Hunter et al in 1993, which compared the neonatal morbidity among infants of 230 women with insulin-dependent diabetes and infants of 460 women without diabetes. The infants of diabetic mothers (IDMs) had 5-fold higher rates of severe hypoglycemia, a 4-fold increase in macrosomia, and a doubled increase in neonatal jaundice.
      • Birth injury, including shoulder dystocia and brachial plexus trauma, are more common among infants of diabetic mothers, and macrosomic fetuses are at the highest risk.
      • The macrosomic fetus in diabetic pregnancy develops a unique pattern of overgrowth, involving central deposition of subcutaneous fat in the abdominal and interscapular areas. Skeletal growth is largely unaffected. Neonates of diabetic mothers have a larger shoulder and extremity circumference, a decreased head-to-shoulder ratio, significantly higher body fat and thicker upper extremity skin folds compared to nondiabetic control infants of similar weights. Since fetal head size is not increased during poorly controlled diabetic pregnancy but shoulder and abdominal girth can be markedly augmented, the risk of injury to the fetus after delivery of the head (eg Erb palsy) is significantly increased.
      • When serial ultrasound examination findings from diabetic fetuses are plotted, the growth velocity of the abdominal circumference is often well above the growth centiles seen in nondiabetic fetuses and is higher than the fetal head and femur centiles. The accelerated growth of the abdominal circumference begins to rise significantly above normal after 24 weeks.
    • Metabolic syndrome
      • The adverse downstream effects of abnormal maternal metabolism on the offspring have been documented well into puberty. Glucose intolerance and higher serum insulin levels are more frequent in children of diabetic mothers as compared to normal controls. By age 10-16 years, offspring of diabetic pregnancy have a 19.3% rate of impaired glucose intolerance.
      • The childhood metabolic syndrome includes childhood obesity, hypertension, dyslipidemia, and glucose intolerance. A growing body of literature supports a relationship between intrauterine exposure to maternal diabetes and risk of a metabolic syndrome later in life.
      • Fetuses of diabetic women that are born large for gestational age appear to be at the greatest risk.
    • Role of glucose levels
      • Excess nutrient delivery to the fetus causes macrosomia and truncal fat deposition, but whether fasting or peak glucose values are more correlated with fetal overgrowth is less clear.
      • Data from the Diabetes in Early Pregnancy project indicate that fetal birthweight correlates best with second- and third-trimester postprandial blood sugar levels and not with fasting or mean glucose levels.17
      • More recent data from the ACHOIS trial demonstrated a positive relationship between severity of maternal fasting hyperglycemia and risk of shoulder dystocia, with a 1 mmol increase in fasting glucose leading to a relative risk for shoulder dystocia of 2.09 (1.03- 4.25).18
      • When postprandial glucose values average 120 mg/dL or less, approximately 20% of infants can be expected to be macrosomic. When postprandial levels range as high as 160 mg/dL, macrosomia rates can reach 35%.
      • In addition, there appears to be a role for excessive fetal insulin levels in mediating accelerated fetal growth. In the study by Simmons et al which compared umbilical cord sera in infants of diabetic mothers newborns and controls, the heavier, fatter babies from diabetic pregnancies were also hyperinsulinemic.19
    • Role of maternal obesity
      • Maternal obesity has a strong and independent effect on fetal macrosomia. Birthweight is largely determined by maternal factors other than hyperglycemia, with the most significant influences being gestational age at delivery, prepregnancy maternal body mass index (BMI), maternal height, pregnancy weight gain, the presence of hypertension, and cigarette smoking.
      • When women who are very obese (weight >300 lb) were compared to women of normal weight, the obese women had more than double the risk of macrosomia compared to the women who were of normal weight. This may explain the failure of glycemic control to completely prevent fetal macrosomia in several series.
  • Perinatal morbidity and birth injury
    • Perinatal mortality
      • In diabetic pregnancy, perinatal mortality has decreased 30-fold since the discovery of insulin in 1922 and intensive obstetrical and infant care in the 1970s. Nevertheless, the current perinatal mortality rates among women who are diabetic remain approximately twice those observed in the nondiabetic population.
      • Congenital malformations, respiratory distress syndrome (RDS), and extreme prematurity account for most perinatal deaths in contemporary diabetic pregnancies.
Table 1. Perinatal Morbidity in Diabetic Pregnancy


Gestational Diabetes

Type 1 Diabetes

Type 2 Diabetes









Respiratory distress




Transient tachypnea
















Adapted from California Department of Health Services, 1991
    • Birth injury
      • Injuries of birth, including shoulder dystocia and brachial plexus trauma, are more common among infants of diabetic mothers, and macrosomic fetuses are at the highest risk.
      • Most of the birth injuries occurring to infants of diabetic mothers are associated with difficult vaginal delivery and shoulder dystocia. While shoulder dystocia occurs in 0.3-0.5% of vaginal deliveries among healthy pregnant women, the incidence is 2- to 4-fold higher in women with diabetes. With strict glycemic control, the birth injury rate has been shown to be only slightly higher than controls (3.2 vs 2.5%).
      • Currently, clinical ability to predict shoulder dystocia is poor. Warning signs during labor (labor protraction, suspected fetal macrosomia, need for operative vaginal delivery) successfully predict only 30% of these events.
      • Common birth injuries associated with diabetes are brachial plexus, facial nerve injury, and cephalohematoma.
    • Polycythemia
      • A central venous hemoglobin concentration greater than 20 g/dL or a hematocrit value greater than 65% (polycythemia) is not uncommon in infants of diabetic mothers and is related to glycemic control.
      • Hyperglycemia is a powerful stimulus to fetal erythropoietin production mediated by decreased fetal oxygen tension.
      • Untreated neonatal polycythemia may promote vascular sludging, ischemia, and infarction of vital tissues, including the kidneys and central nervous system.
    • Hypoglycemia
      • Approximately 15-25% of neonates delivered from women with diabetes during gestation develop hypoglycemia during the immediate newborn period.20 Neonatal hypoglycemia is less frequent when tight glycemic control is maintained during pregnancy21 and in labor.
      • Unrecognized postnatal hypoglycemia may lead to neonatal seizures, coma, and brain damage.
    • Neonatal hypocalcemia
      • Up to 50% of infants of diabetic mothers have low levels of serum calcium (<7>
      • These changes in calcium appear to be attributable to a functional hypoparathyroidism, though the exact pathophysiology is not well understood.
    • Postnatal hyperbilirubinemia
      • Hyperbilirubinemia occurs in approximately 25% of infants of diabetic mothers, a rate approximately double that in a healthy population. The causes of hyperbilirubinemia in infants of diabetic mothers are multiple, but prematurity and polycythemia are the primary contributing factors. Increased destruction of red blood cells contributes to the risk of jaundice and kernicterus.
      • Treatment of this complication is usually by phototherapy, but exchange transfusions may be necessary if bilirubin levels are markedly elevated.
    • Respiratory problems
      • Until recently, neonatal respiratory distress syndrome (RDS) was the most common and serious morbidity in infants of diabetic mothers. In the 1970s, improved prenatal maternal management for diabetes and new techniques in obstetrics for timing and mode of delivery resulted in a dramatic decline in its incidence from 31% to 3%.22 Nevertheless, respiratory distress syndrome continues to be a relatively preventable complication.
      • The majority of the literature indicates a significant biochemical and physiological delay in infants of diabetic mothers. Tyden23 and Landon24 and colleagues reported that fetal lung maturity occurred later in pregnancies with poor glycemic control regardless of class of diabetes when infants were stratified by maternal plasma glucose levels.
      • The nondiabetic fetus achieves pulmonary maturity at a mean gestational age of 34-35 weeks. By 37 weeks’ gestation, more than 99% of healthy newborn infants have mature lung profiles as assessed by phospholipid assays. However, in a diabetic pregnancy, presuming that the risk of respiratory distress has passed is unwise until after 38.5 gestational weeks have been completed.
      • Prior to contemplating any delivery before 38.5 weeks for other than the most urgent fetal and maternal indications, perform an amniocentesis to document pulmonary maturity.
  • Maternal morbidity
    • Diabetic retinopathy
      • This is the leading cause of blindness in women aged 24-64 years. Some form of retinopathy is present in virtually 100% of women who have had type 1 diabetes for 25 years or more; of these women, approximately 1 in 5 is legally blind.
      • A prospective study showed that while half the patients with preexisting retinopathy experienced deterioration during pregnancy, all the patients had partial regression following delivery and returned to their prepregnant state by 6 months postpartum.
      • Other studies have suggested that rapid induction of glycemic control in early pregnancy stimulates retinal vascular proliferation.25 However, when the total effect of pregnancy on ophthalmologic status was considered, women with pregnancies had a slower progression of retinopathy than nonpregnant women, probably because the modest deterioration in retinal status during rapid improvement in control is offset by the excellent control during the remainder of the pregnancy.
      • Current management recommendations include baseline ophthalmology referral for pregnant patients with diabetes, with follow-up according to degree of retinopathy.
    • Renal function
      • In general, patients with underlying nephropathy can expect varying degrees of deterioration of renal function during a pregnancy. As renal blood flow and glomerular filtration rate increase 30-50% during pregnancy, the degree of proteinuria will also increase.
      • The most recent studies indicate that pregnancy does not measurably alter the time course of diabetic renal disease, nor does it increase the likelihood of progression to end stage renal disease. The progression to renal disease in diabetic patients appears to be related to duration of diabetes and degree of glycemic control.
      • Patients using the subcutaneous insulin pump have lower mean glucose levels than those using intermittent injections. The effect on progression of nephropathy of 2 years of strict metabolic control showed that none of the patients managed on the insulin pump progressed to clinical nephropathy, while 5 patients with conventional treatment did.
      • Perinatal complications are greatly increased in patients with diabetic nephropathy. Preterm birth, intrauterine growth restriction, and preeclampsia are all significantly more common in women with diabetic nephropathy during pregnancy.
    • Chronic hypertension
      • This complicates approximately 1 in 10 diabetic pregnancies overall. Patients with underlying renal or retinal vascular disease are at a substantially higher risk, with 40% having chronic hypertension.
      • Patients with chronic hypertension and diabetes are at increased risk of intrauterine growth restriction, superimposed preeclampsia, abruptio placentae, and maternal stroke.
      • Baseline renal function determination is recommended in all patients with preexisting diabetes. Renal function assessments in each trimester should be performed in those with overt vascular disease or who have had diabetes for more than 10 years.
    • Preeclampsia
      • Consists of abrupt elevation in blood pressure, significant proteinuria, plasma uric acid levels greater than 6 mg/dL or evidence of hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome.
      • Preeclampsia is more frequent among women with diabetes, occurring in approximately 12% as compared to 8% of the nondiabetic population. The risk of preeclampsia is also related to maternal age and the duration of preexisting diabetes. In patients who have chronic hypertension coexisting with diabetes, preeclampsia may be difficult to distinguish from near-term blood pressure elevations.
      • The rate of preeclampsia has been found to be related to the level of glycemic control, with fasting plasma glucose (FPG) less than 105, the rate of preeclampsia was 7.8%, if FPG was greater than 105, the rate of preeclampsia was 13.8%.26
      • In this same study, pregravid body mass index was also significantly related to the development of preeclampsia.
Risk for Developing Gestational Diabetes
Some of the most common risks for developng gestational diabetes are:
  • A family history of diabetes in parents or brothers and sisters.
  • Gestational diabetes in a previous pregnancy
  • the presence of o birth defect in a previous pregnancy
  • obesity in the women.BMI greather than 29
  • older mathernal age(over the age of 30)
  • previous delivery of large baby(4 kg or more)
  • A history of pregnancy induced high blood pressure,urinary tract infections,hydramnions(extra amniotic fluids)
  • Race :women of hispanic ,asian,african-american decent.

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posted by Bunda at 14:54 | Permalink | 1 comments
Wednesday, 18 June 2008
Type 2 diabetes is sometimes described as a ‘lifestyle disease’ because it is more common in people who do insufficient physical activity and are overweight or obese. It is strongly associated with high blood pressure, high cholesterol and an ‘apple’ body shape, where excess weight is carried around the waist.
Type 2 diabetes is by far the most common form of diabetes. It affects 85 to 90 per cent of all people with diabetes. While it usually affects mature adults, younger people are also now being diagnosed in greater numbers as rates of overweight and obesity increase.Type 2 diabetes used to be called non-insulin dependent diabetes(NIDDM) or mature onset diabetes.
he body uses glucose as its main source of energy. Glucose comes from foods that contain carbohydrates. After food is digested, the glucose is released and absorbed into the bloodstream.
The glucose in the bloodstream needs to move into body tissues so that cells can use it for energy. Excess glucose is also stored in the liver or converted to fat and stored in other body tissues.
Insulin is a hormone made by the pancreas, which is a gland located just below the stomach. Insulin opens the doors (the glucose channels) that let glucose move from the blood into the body cells. This is part of a process known as glucose metabolism.
In diabetes, one of two things occurs.
The pancreas can’t make insulin (type 1 diabetes) or the cells don’t respond to the insulin properly (insulin resistance) and the pancreas produces inadequate insulin for the body’s increased needs (type 2 diabetes).
If the insulin can’t do its job, the glucose channels can’t open properly and glucose builds up in the blood. High blood glucose levels cause the health problems linked to diabetes, often referred to as complications.

Risk Factor of Type 2 Diabetes
Research don't fully understand why some people develop type 2 diabetes and others don;ts.it's clear that certain factors increase the rusk,however,including:
  • Obesity ; being overweight is a primary risk faktor for type 2 diabetes.the more fatty tissue you have,the more resistant your cells beccome to insulin.
  • Gestational Diabetes Millitus (DM during pregnancy) or large baby (over 4kg) ; if you develeop gestatioanl diabets when you are pregnant or if you gave birth to a baby weighing more than 4kg, your risk of developing type 2 diabetes later increase.
  • Family History of diabetes millitus ; if a parents or sibling has type 2 diabetes also the risk you will get type 2 diabetes.
  • Cardiovascular disease and cerebrovascular disease ; any problem in the heart is risk to get diabetes type 2 including hypertension,ischemich heart attack,peripheal vascular disease.
  • Race ; Althuogh it's unclear why,people of certain races-including blacks african-carribbean origin,hispanics and asian are more likely to develop type 2 diabetes.
  • Age ; the risk type 2 diabetes increases as you get older.especially after age 45.often,that's because people tend to exercise ,lose muscle mass and gain weight as they age.but type 2 diabetes increasing dramatically among children,adolescent ang younger adults.
  • Inactivity ; the less active you are,the greater your risk of type 2 diabets.phisical activity helps you control your weight,uses up glucose as energy and makes your cells more sensitive to insulin.
  • Pre diabetes ; when your blood sugar red limit.is mean more than normal but not enough to be idntifiead as type 2 diabetes.left untreated,prediabetes often progresses to type 2 diabetes.
Sign and Symptoms

Type 2 diabetes usually begins gradually and progresses slowly. Symptoms in adults include:

  • Excessive thirst(Polydipsia) As excess sugaf builds up in your blood stream,fluid is pulled from your tissue.this may leave you thirsty
  • Increased urination(polyuria) As a result thirsty,you may drink more.so that urinate more than usual
  • Extreme hunger(Polypagia)Without enough insulin to move sugar into your cells.your muscles and organs become depleted of energy.this triggers intense hunger thay may persisit eveb after eating.
  • Fatigue.if the cells are deprived of sugar,become tired and irritable
  • Blurred vision ig blood sugar level is too high fluid pulled from the tissue- including the lenses of eyes.this make affect ability to focus.
  • Weight loss.despite eatning more tha usual to relieve hunger,may lose weight.without energy the energy sugar supplies,muscles tissue and fat stores may simply shrink.
  • In women, vaginal yeast infections or fungal infections under the breasts or in the groin
  • Severe gum problems
  • Itching
  • Erectile dysfunction in men
  • Slow-healing sores or frequent infections.type 2 diabetes affects abilty to heal and fight infections.
  • Macrovascular complications often present.microvascular comlications may be present

Symptoms in children are often different:

  • Most children are obese or overweight
  • Increased urination is mild or even absent
  • Many children develop a skin problem called acanthosis, characterized by velvety, dark colored patches of skin
Diagnosis and testing
Usually discovered when a patient presents to the physician for some other related symptoms.Various blood tests can be used to screen for diabetes, including:
  • Random blood sugar test. A blood sample will be taken at a random time. Regardless of when you last ate, a random blood sugar level of 200 milligrams per deciliter (mg/dL) or higher suggests diabetes.
  • Fasting blood sugar test. A blood sample will be taken after an overnight fast. A fasting blood sugar level between 70 and 100 mg/dL is normal. A fasting blood sugar level from 100 to 125 mg/dL is considered prediabetes, which indicates a high risk of developing diabetes. If it's 126 mg/dL or higher on two separate tests, you'll be diagnosed with diabetes.it is a simple blood test taken after 8 hours of fasting
  • Oral Glucose Tolerance Test(OGTT) is more complex than the FBS and may overdiagnose diabetes in people who do no have it. some expert recommend it as a follow-up after FBS. if the later test result are normal but the patient has symptoms or risk factors of diabetes.GTT prosedure : the patien first has an FBS and take again after 2 hours drinking a special glucose solution.OGTT levels are considered normal up to 140 mg/dl.pre diabetes 140-199 mg/dl and higher 200 mg/dl are diabetes.
  • Post Prandial Blood sugar (PPBS) taken after 2 hours eating
  • Glycostated Hemoglobi(HBA1C) is a form of hemoglobin used primarily to identify the avarege Plasma glucose concentration over prolonged periods of time ( within 3 months ) .HBA1C are not used for an initial diagnosis but they are usefull for determining the severity of diabetes.
Screening Tests for Complications
  • Screening for Heart Disease. All patients with diabetes should be tested for hypertension and unhealthy cholesterol and lipid levels and given an electrocardiogram. For cholesterol, people with diabetes should aim for LDL levels below 100 mg/dL, HDL levels over 50 mg/dL, and triglyceride levels below 150 mg/dL. Blood pressure goals should be 130/80 mm Hg or lower. Other tests may be needed in patients with signs of heart disease.
  • The electrocardiogram (ECG or EKG) is used extensively in the diagnosis of heart disease, from congenital heart disease in infants to myocardial infarction and myocarditis in adults. Several different types of electrocardiogram exist.
  • Screening for Kidney Damage. The earliest manifestation of kidney damage is microalbuminuria, in which tiny amounts (30 - 300 mg per day) of protein called albumin are found in the urine. About 20% of type 2 patients show evidence of microalbuminuria upon diagnosis of diabetes. (However, not all people with type 2 diabetes eventually develop kidney disease.) Microalbuminuria typically shows up in patients with type 2 diabetes who have high blood pressure.people with diabetes receive an annual microalbuminuria urine test. Patients should also have their blood creatinine tested at least once a year. Creatinine is a waste product that is removed from the blood by the kidneys. High levels of creatinine may indicate kidney damage. A doctor uses the results from a creatinine blood test to calculate the glomerular filtration rate (GFR). The GFR is an indicator of kidney function; it estimates how well the kidneys are cleansing the blood.
  • Screening for Retinopathy.patients with type 2 diabetes get an initial comprehensive eye exam by an ophthalmologist or optometrist shortly after they are diagnosed with diabetes, and once a year thereafter. (People at low risk may need follow-up exams only every 2 - 3 years.) The eye exam should include dilation to check for signs of retinal disease (retinopathy).
  • Screening for Neuropathy. All patients should be screened for nerve damage (neuropathy), including a comprehensive foot exam. Patients who lose sensation in their feet should have a foot exam every 3 - 6 months to check for ulcers or infections.
  • Screening for Thyroid Abnormalities. Thyroid function tests( TFT ) should be administered.
Dietary Goals and Exercise


The treatment goals for a diabetes diet are:
  • Achieve near-normal blood glucose levels. People with type 1 diabetes must coordinate calorie intake with medication or insulin administration, exercise, and other variables to control blood glucose levels. New forms of insulin now allow more flexibility in timing meals.
  • Protect the heart and aim for healthy lipid (cholesterol and triglyceride) levels and control of blood pressure.
  • Achieve reasonable weight. A reasonable weight is usually defined as a weight that is achievable and sustainable, rather than one that is culturally defined as desirable or ideal. Children, pregnant women, and people recovering from illness should be sure to maintain adequate calories for health.
  • Manage or prevent complications of diabetes. People with diabetes, whether type 1 or 2, are at risk for a number of medical complications, including heart and kidney disease. Dietary requirements for diabetes must take these disorders into consideration.
  • Promote overall health.

Overall Guidelines. There is no such thing as a single diabetes diet. Patients should meet with a professional dietitian to plan an individualized diet within the general guidelines that takes into consideration their own health needs.

Healthy eating habits along with good control of blood glucose are the basic goals, and several good dietary methods are available to meet them. General dietary guidelines for diabetes recommend:

  • Carbohydrates should provide 45 - 65% of total daily calories. The type and amount of carbohydrate are both important. Best choices are vegetables, fruits, beans, and whole grains. These foods are also high in fiber. Patients with diabetes should monitor their carbohydrate intake either through carbohydrate counting or meal planning exchange lists.
  • Fats should provide 25 - 35% of daily calories. Monounsaturated (olive, peanut, and canola oils; avocados; nuts) and omega-3 polyunsaturated (fish, flaxseed oil, and walnuts) fats are the best types. Limit saturated fat (red meat, butter) to less than 7% of daily calories. Choose nonfat or low-fat dairy instead of whole milk products. Limit trans-fats (hydrogenated fat found in snack foods, fried foods, commercially baked goods) to less than 1% of total calories.
  • Protein should provide 12 - 20% of daily calories, although this may vary depending on a patient’s individual health requirements. Patients with kidney disease should limit protein intake to less than 10% of calories. Fish, soy, and poultry are better protein choices than red meat.

Weight Management

Being overweight is the number one risk factor for type 2 diabetes. Even modest weight loss can help prevent type 2 diabetes from developing. It can also help control or even stop progression of type 2 diabetes in people with the condition and reduce risk factors for heart disease. Patients should lose weight if their body mass index (BMI) is 25 - 29 (overweight) or higher (obese).

The American Diabetes Association recommends that patients aim for a small but consistent weight loss of ½ - 1 pound per week. Most patients should follow a diet that supplies at least 1,000 - 1,200 kcal/day for women and 1,200 - 1,600 kcal/day for men.

Unfortunately, not only is weight loss difficult to sustain, but many of the oral medications used in type 2 diabetes cause weight gain as a side effect. For obese patients who cannot control weight using dietary measures alone, weight-loss drugs, such as orlistat (Xenical) or sibutramine (Meridia), may be helpful. Orlistat may have specific benefits for people with diabetes. It may not only help achieve weight but also improve glucose, cholesterol, and lipid levels. In 2007, the FDA approved a non-prescription form of orlistat (alli). [For more information, see In-Depth Report #53: Obesity.]


Sedentary habits, especially watching TV, are associated with significantly higher risks for obesity and type 2 diabetes. Regular exercise, even of moderate intensity (such as brisk walking), improves insulin sensitivity and may play a significant role in preventing type 2 diabetes -- regardless of weight loss. An important study reported a 58% lower risk for type 2 diabetes in adults who performed moderate exercise for as little as 2.5 hours a week.

Aerobic Exercise. Aerobic exercise has significant and particular benefits for people with diabetes. Regular aerobic exercise, even of moderate intensity, improves insulin sensitivity. People with diabetes are at particular risk for heart disease, so the heart-protective effects of aerobic exercise are especially important. Moderate exercise protects the heart in people with type 2 diabetes, even if they have no risk factors for heart disease other than diabetes itself.

For improving glycemic control, the American Diabetes Association recommends at least 150 minutes per week of moderate-intensity physical activity (50 - 70% of maximum heart rate) or at least 90 minutes per week of vigorous aerobic exercise (more than 70% of maximum heart rate). Exercise at least 3 days a week, and do not go more than 2 consecutive days without physical activity.

Strength Training. Strength training, which increases muscle and reduces fat, is also helpful for people with diabetes who are able to do this type of exercise. The American Diabetes Association recommends performing resistance exercise three times a week. Build up to three sets of 8 - 10 repetitions using weight that you cannot lift more than 8 - 10 times without developing fatigue. Be sure that your strength training targets all of the major muscle groups.

Exercise Precautions. The following are precautions for all people with diabetes, both type 1 and type 2:

  • Because people with diabetes are at higher than average risk for heart disease, they should always check with their doctors before undertaking vigorous exercise. For fastest results, frequent high-intensity (not high-impact) exercises are best for people who are cleared by their doctors. For people who have been sedentary or have other medical problems, lower-intensity exercises are recommended.
  • Strenuous strength training or high-impact exercise is not recommended for people with uncontrolled diabetes. Such exercises can strain weakened blood vessels in the eyes of patients with retinopathy. High-impact exercise may also injure blood vessels in the feet.

Patients who are taking medications that lower blood glucose, particularly insulin, should take special precautions before embarking on a workout program:

  • Monitor glucose levels before, during, and after workouts (glucose levels swing dramatically during exercise).
  • Avoid exercise if glucose levels are above 300 mg/dL or under 100 mg/dL.
  • Inject insulin in sites away from the muscles used during exercise; this can help avoid hypoglycemia.
  • Drink plenty of fluids before and during exercise; avoid alcohol, which increases the risk of hypoglycemia.
  • Insulin-dependent athletes may need to decrease insulin doses or take in more carbohydrates prior to exercise, but may need to take an extra dose of insulin after exercise (stress hormones released during exercise may increase blood glucose levels).
  • Wear good, protective footwear to help avoid injuries and wounds to the feet.
  • Some blood pressure drugs can interfere with exercise capacity. Patients who use blood pressure medication should talk to their doctors about how to balance medications and exercise. Patients with high blood pressure should also aim to breathe as normally as possible during exercise. Holding the breath can increase blood pressure

Pre-diabetes precedes the onset of type 2 diabetes. People who have pre-diabetes have fasting blood glucose levels that are 100 - 125 mg/dL -- higher than normal, but not yet high enough to be classified as diabetes. (Pre-diabetes used to be referred to as “impaired glucose tolerance.”) Pre-diabetes greatly increases the risk for diabetes.

Treatment of pre-diabetes is very important. Research shows that lifestyle and medical interventions can help prevent, or at least delay, the progression to diabetes. While doctors sometimes prescribe insulin-regulating drugs such as metformin (Glucophage) and acarbose (Precose), evidence indicates that lifestyle changes can be at least as effective as drug therapy. The most important lifestyle treatment for people with pre-diabetes is to lose weight through diet and regular exercise. Even a modest weight loss of 10 - 15 pounds can significantly reduce the risk of progressing to diabetes.

Because people with pre-diabetes have a higher risk for heart disease and stroke, diet and exercise are also very important for heart health, as is quitting smoking. It is also important to have your doctor check your cholesterol and blood pressure levels on a regular basis. Your doctor should also check your fasting blood glucose levels every 1 - 2 years.

The major treatment goals for people with type 2 diabetes are:

  • Treat all conditions that place patients at risk for heart disease and stroke, the major killers of people with type 2 diabetes.
  • Control blood glucose levels. The goal is to achieve fasting blood glucose levels of less than 110 mg/dL and glycosylated hemoglobin (HbA1c) levels of less than 7%. The objective is to reduce complications in small blood vessels and the nerve damage associated with diabetes.
  • In general, most people with type 2 diabetes should aim for HbA1c levels of less than 7%. However, patients who have heart disease or cardiovascular risk factors should talk to their doctor about individualized treatment goals for intensive blood sugar control.

An intensive multi-pronged approach is critical for reducing complications and improving survival rates in patients with diabetes. Intensive therapy includes:

  • Healthy lifestyle changes: Regular exercise, heart-healthy diet, quitting smoking.
  • Controlling blood sugar levels. Monitor blood sugar and hemoglobin HbA1c levels. Oral anti-hyperglycemic drugs such as metformin are first-line drug treatments. Insulin may eventually be needed.
  • Heart-protective drugs. These medications include various drugs to control high blood pressure (such as ACE inhibitors and diuretics) and cholesterol (statins and fibrates). Controlling high blood pressure is a proven factor in reducing mortality rates. Aspirin helps prevent blood clots and heart attack.
  • glycemic control trough a combination of accurate monituring,diet, exercise,oral medicine and or insulin therapy
  • HBA1C less than 7 %
  • Cholesterol less than 4 mmol/L
  • HDL-C more than 1 mmol/L
  • LDL-C less than 2 mmol?L
  • Triglycerides less than 1.5 mmol/L

Many anti-hyperglycemic drugs are available to help patients with type 2 diabetes control their blood sugar levels. Most of these drugs are aimed at using or increasing sensitivity to the patient's own natural stores of insulin. Metformin is the only drug to date that achieves lower mortality rates.

For the most part older oral hypoglycemic drugs -- such as metformin and sulfonylureas -- are less expensive than, and work as well as, newer diabetes drugs. They are generally recommended as first-line drugs to use. Metformin is a safe and effective drug because it does not cause weight gain or too-low blood sugar. Metformin can also help lower LDL (“bad”) cholesterol.

In general, these drugs will reduce hemoglobin A1c levels by 1 - 2%. Adding a second oral hypoglycemic is generally recommended if inadequate control is not achieved with the first medication. For the most part, doctors should add a second drug rather than trying to push the first drug dosage to the highest levels.

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posted by Bunda at 15:33 | Permalink | 0 comments
Tuesday, 17 June 2008
Diabetes is a lifelong disease for which there is not yet a cure. There are several forms of diabetes. Type 1 diabetes, also called juvenile diabetesorinsulin-dependent diabetes(IDDM), is a disorder of the body's immune system -- that is, its system for protecting itself from viruses, bacteria or any "foreign" substances. A third form of diabetes, called monogenic diabetes, is sometimes mistaken for type 1 diabetes.
Type 1 diabetes occurs when the body's immune system attacks and destroys certain cells in the pancreas, an organ about the size of a hand that is located behind the lower part of the stomach.
These cells -- called beta cells -- are contained,along with other types of cells, within small islands of endocrine cells called the pancreatic islets. Beta cells normally produce insulin, a hormone that helps the body move the glucose contained in food into cells throughout the body, which use it for energy. But when the beta cells are destroyed, no insulin can be produced, and the glucose stays in the blood instead, where it can cause serious damage to all the organ systems of the body.
Without enough insulin, glucose builds up in the bloodstream instead of going into the cells. The body is unable to use this glucose for energy despite high levels in the bloodstream. This leads to increased hunger.
this case the cells that make insulin (the beta cells) are damaged.
in addition, the high levels of glucose in the blood cause the patient to urinate more, which in turn causes excessive thirst. Within 5 to 10 years, the insulin-producing beta cells of the pancreas are completely destroyed and the body can not longer produce insulin.
Type 1 Diabetes less common from affecting 10% of diabtetes cases.
The cause of type 1 diabetes remains unknown. However, it is not preventable, and it is not caused by eating too much sugar. The body's defense system may attack insulin-making cells by mistake, but we don't know why. People are usually diagnosed with type 1 diabetes before the age of 30, most often during childhood or their teens.

Caused of type 1 diabetes

there is no specific cause can be identified.
some of the theories are:
  • Genetic
  • carry a gene Enviromental
  • viruses
  • auto immun disorede
  • accident causing pancreas broken and can not produce insulin anymore
Sign and Symptomps
Exam and Test
  • The need for and extent of laboratory studies vary, depending upon the general state of the child's health. For most children, only urine testing for glucose and blood glucose measurement are required for a diagnosis of diabetes. Other conditions associated with diabetes require several tests at diagnosis and at later review. (See Diabetic Ketoacidosis for information on laboratory studies needed to manage cases of DKA.)
  • Urine glucose
    • A positive urine glucose test suggests but is not diagnostic for IDDM. Diagnosis must be confirmed by test results showing elevated blood glucose levels.
    • Test urine of ambulatory patients for ketones at the time of diagnosis.
  • Urine ketones
    • Ketones in the urine confirm lipolysis and gluconeogenesis, which are normal during periods of starvation.
    • With hyperglycemia and heavy glycosuria, ketonuria is a marker of insulin deficiency and potential DKA.
  • Blood glucose
    • Apart from transient illness- or stress-induced hyperglycemia, a random whole-blood glucose concentration more than 200 mg/dL (11 mmol/L) is diagnostic for diabetes, as is a fasting whole-blood glucose concentration exceeding 120 mg/dL (7 mmol/L). In the absence of symptoms, the physician must confirm these results on a different day. Most children with diabetes detected because of symptoms have a blood glucose level of at least 250 mg/dL (14 mmol/L).
    • Blood glucose tests using capillary blood samples, reagent sticks, and blood glucose meters are the usual methods for monitoring day-to-day diabetes control.
  • Glycated hemoglobin
    • Glycosylated hemoglobin derivatives (HbA1a, HbA1b, HbA1c) are the result of a nonenzymatic reaction between glucose and hemoglobin. A strong correlation exists between average blood-glucose concentrations over an 8- to 10-week period and the proportion of glycated hemoglobin. The percentage of HbA1c is more commonly measured. Normal values vary according to the laboratory method used, but nondiabetic children generally have values in the low-normal range. At diagnosis, diabetic children unmistakably have results above the upper limit of the reference range.
    • Measurement of HbA1c levels is the best method for medium- to long-term diabetic control monitoring. The Diabetes Control and Complications Trial (DCCT) has demonstrated that patients with HbA1c levels around 7% had the best outcomes relative to long-term complications. Check HbA1c levels every 3 months. Most clinicians aim for HbA1c values of 7-9%. Values less than 7% are associated with an increased risk of severe hypoglycemia; values more than 9% carry an increased risk of long-term complications.
  • Renal function tests: If the child is otherwise healthy, renal function tests are typically not required.
  • Islet cell antibodies
    • Islet cell antibodies may be present at diagnosis but are not needed to diagnose IDDM.
    • Islet cell antibodies are nonspecific markers of autoimmune disease of the pancreas and have been found in as many as 5% of unaffected children. Other autoantibody markers of type 1 diabetes are known, including insulin antibodies. More antibodies against islet cells are known (eg, those against glutamate decarboxylase [GAD antibodies]), but these are generally unavailable for routine testing.
  • Thyroid function tests
    • Because early hypothyroidism has few easily identifiable clinical signs in children, children with IDDM may have undiagnosed thyroid disease.
    • Untreated thyroid disease may interfere with diabetes management. Check thyroid function regularly (every 2-5 years or annually if thyroid antibodies are present).
  • Antithyroid antibodies: This test indicates risk of present or potential thyroid disease.
  • Antigliadin antibodies
    • Some children with IDDM may have or develop celiac disease. Positive antigliadin antibodies, especially specific antibodies (eg, antiendomysial, antitransglutaminase) are important risk markers.
    • If antibody tests are positive, a jejunal biopsy is required to confirm or refute a diagnosis of celiac disease.
Other test are needed
  • Oral glucose tolerance test (OGTT)
    • While unnecessary to diagnose IDDM, an OGTT can exclude the diagnosis of diabetes when hyperglycemia or glycosuria are recognized in the absence of typical causes (eg, intercurrent illness, steroid therapy) or when the patient's condition includes renal glucosuria.
    • Obtain a fasting blood sugar level, then administer a PO glucose load (2 g/kg for children aged <3>10 y). Check the blood glucose concentration again after 2 hours. A fasting whole-blood glucose level higher than 120 mg/dL (6.7 mmol/L) or a 2-hour value higher than 200 mg/dL (11 mmol/L) indicates diabetes. Mild elevations, however, may not indicate diabetes when the patient has no symptoms and no diabetes-related antibodies.
    • A modified OGTT can also be used to identify cases of MODY that often present as type 1 diabetes, if, in addition to blood glucose levels, insulin or c-peptide (insulin precursor) levels are measured at fasting, 30 minutes, and 2 hours. Type 1 diabetics cannot produce more than tiny amounts of insulin. People with MODY or type 2 diabetes show variable and substantial insulin production in the presence of hyperglycemia.
  • Lipid profile
    • Lipid profiles are usually abnormal at diagnosis because of increased circulating triglycerides caused by gluconeogenesis.
    • Apart from hypertriglyceridemia, primary lipid disorders rarely result in diabetes.
    • Hyperlipidemia with poor metabolic control is common.
  • Urinary albumin: Beginning at age 12 years, perform an annual urinalysis to test for a slightly increased albumin excretion rate (AER), referred to as microalbuminuria, which is an indicator of risk for diabetic nephropathy.
Taking Care of of Type 1 Diabetes
Because pancreas is not longer produce insulin any more or luck of insulin is mean blood glucose almost always high to very high.so we can manage action
-Growth assesment
-managing injection dose
-retinoscopy or other retinal screening such as Photografi
-Examination of hands,feet,and peripheral pulses for sign of limited joint mobility,peripheral neuropaty,and vascular disease
-Evaluation for sign of associated autoimmune disease
-check Blood pressure
-urine Examination for microalbumine
Medical Care
  • All children with IDDM require insulin therapy.
  • Only children with significant dehydration, persistent vomiting, or metabolic derangement, or with serious intercurrent illness, require inpatient management and intravenous rehydration.
  • A well-organized diabetes care team can provide all necessary instruction and support in an outpatient setting. The only immediate requirement is to train the child or family to check blood glucose levels, to administer insulin injections, and to recognize and treat hypoglycemia. The patient and/or family should have 24-hour access to advice and know how to contact the team.
  • Always involve an experienced dietitian in the patient's care, typically as a regular member of the diabetes care team.
  • Ophthalmology review may be needed at diagnosis if a cataract is suspected. All children with diabetes aged 12 years and older need a careful annual eye examination, either by direct ophthalmoscopy or high-quality retinal photography to identify and, if necessary, treat diabetes-related eye complications.
  • Access to psychological counseling and support is desirable, preferably from a member of the diabetes care team.


Dietary management is an essential component of diabetes care. Diabetes is an energy metabolism disorder, and before insulin was discovered, children with diabetes could be kept alive by a diet severely restricted in carbohydrate and energy intake. These measures led to a long tradition of strict carbohydrate control and unbalanced diets. More recent dietary management of diabetes emphasizes a healthy, balanced diet, high in carbohydrates and fiber and low in fat.

  • The following are universal recommendations:
    • Carbohydrates should provide 50-60% of daily energy intake. (No more than 10% of carbohydrates should be from sucrose or other refined carbohydrates.)
    • Fat should provide less than 30%.
    • Protein should provide 10-20%.
    • View these recommendations in the patient's cultural context.
  • The aim of dietary management is to balance the child's food intake with insulin dose and activity and to keep blood glucose concentrations as close as possible to reference ranges, avoiding extremes of hyperglycemia and hypoglycemia.
  • The ability to estimate the carbohydrate content of food (carb counting) is particularly useful for those children who give fast-acting insulin at meal times either by injection or insulin pump, as it allows for a more precise matching of food and insulin.
    • Adequate intake of complex carbohydrates (eg, cereals) is important before bedtime to avoid nocturnal hypoglycemia, especially for children having twice-daily injections of mixed insulin.
    • The dietitian should develop a diet plan for each child to suit individual needs and circumstances. Regularly review and adjust the plan to accommodate the patient's growth and lifestyle changes.
    • Low-carbohydrate diets as a management option for diabetes control have regained popularity in recent years. Logic dictates that the lower the carbohydrate intake, the less insulin is required. No trials of low-carbohydrate diets in children with type 1 diabetes have been reported, and such diets cannot be recommended at the present.
  • IDDM requires no restrictions on activity; exercise has real benefits for a child with diabetes.
  • Most children can adjust their insulin dosage and diet to cope with all forms of exercise.
  • Children and their caretakers must be able to recognize and treat symptoms of hypoglycemia.
    • Hypoglycemia following exercise is most likely after prolonged exercise involving the legs, such as walking, running or cycling. It may occur many hours after exercise has finished and even affect insulin requirements the following day.
    • A large presleep snack is advisable following intensive exercise.
  • Hypoglycemia
    • Hypoglycemia is probably the most disliked and feared complication of diabetes, from the point of view of the child and the family. Children hate the symptoms of a hypoglycemic episode and the loss of personal control it may cause.
    • Insulin inhibits glucogenesis and glycogenolysis, while stimulating glucose uptake. In nondiabetic individuals, insulin production by the pancreatic islet cells is suppressed when blood glucose levels fall below 83 mg/dL (4.6 mmol/L). If insulin is injected in a treated diabetic child who has not eaten adequate amounts of carbohydrates, blood glucose levels progressively fall.
    • The brain depends upon glucose as a fuel. As glucose levels drop below 65 mg/dL (3.2 mmol/L) counterregulatory hormones (eg, glucagon, cortisol, epinephrine) are released, and symptoms of hypoglycemia develop. These symptoms include sweatiness, shaking, confusion, behavioral changes, and, eventually, coma when blood glucose levels fall below 30-40 mg/dL. The glucose level at which symptoms develop varies greatly from individual to individual (and from time to time in the same individual), depending in part on the duration of diabetes, frequency of hypoglycemic episodes, rate of fall of glycemia, and overall control.
    • Manage mild hypoglycemia by giving rapidly absorbed PO carbohydrate or glucose; for a comatose patient, administer an intramuscular injection of the hormone glucagon, which stimulates the release of liver glycogen and releases glucose into the circulation. Where appropriate, an alternative therapy is intravenous glucose (preferably no more than a 10% glucose solution). All treatments for hypoglycemia provide recovery in approximately 10 minutes.
    • Occasionally, a child with hypoglycemic coma may not recover within 10 minutes, despite appropriate therapy. Under no circumstances should further treatment be given, especially intravenous glucose, until the blood glucose level is checked and still found subnormal. Overtreatment of hypoglycemia can lead to cerebral edema and death. If coma persists, seek other causes.
    • Hypoglycemia is a particular concern in children younger than 4 years because the condition may lead to possible intellectual impairment later in life.
  • Hyperglycemia
    • In an otherwise healthy individual, blood glucose levels usually do not rise above 180 mg/dL (9 mmol/L). In a child with diabetes, blood sugar levels rise if insulin is insufficient for a given glucose load. The renal threshold for glucose reabsorption is exceeded when blood glucose levels exceed 180 mg/dL (10 mmol/L), causing glycosuria with the typical symptoms of polyuria and polydipsia.
    • All children with diabetes experience episodes of hyperglycemia.
  • Diabetic ketoacidosis
    • DKA is much less common than hypoglycemia, but it is potentially far more serious, creating a life-threatening medical emergency.
    • Ketosis usually does not occur when insulin is present. In its absence, however, severe hyperglycemia, dehydration, and ketone production contribute to the development of DKA.
  • DKA usually follows increasing hyperglycemia and symptoms of osmotic diuresis. Users of insulin pumps, by virtue of absent reservoirs of subcutaneous insulin, may present with ketosis and more normal blood glucose levels. They are more likely to present with nausea, vomiting, and abdominal pain, symptoms similar to food poisoning.
  • Injection-site hypertrophy
    • If children persistently inject their insulin into the same area, subcutaneous tissue swelling may develop, causing unsightly lumps and adversely affecting insulin absorption. Rotating the injection sites resolves the condition.
    • Fat atrophy can also occur, possibly in association with insulin antibodies. This condition is much less common but more disfiguring.
  • Diabetic retinopathy
    • The most common cause of acquired blindness in many developed nations, diabetic retinopathy is rare in the prepubertal child or within 5 years of onset of diabetes.
    • Prevalence and severity of retinopathy increases with age and is greatest in patients whose diabetic control is poor. Prevalence rates seem to be declining, yet an estimated 80% of people with IDDM develop retinopathy.
    • Diabetic retinopathy's first symptoms are dilated retinal venules and the appearance of capillary microaneurysms, a condition known as background retinopathy. These changes may be reversible or their progression may be halted with improved diabetic control, although some patient's conditions may worsen initially.
    • Subsequent changes in background retinopathy are characterized by increased vessel permeability and leaking plasma that form hard exudates, followed by capillary occlusion and flame-shaped hemorrhages. The patient may not notice these changes unless the macula is involved. Laser therapy may be required at this stage to prevent further visual loss. Proliferative retinopathy follows with further vascular occlusion, retinal ischemia, proliferation of new retinal blood vessels and fibrous tissue, then progressing to hemorrhage, scarring, retinal detachment, and blindness. Prompt retinal laser therapy may prevent blindness in the later stages, so regular screening is vital.
  • Diabetic nephropathy and hypertension
    • Diabetic nephropathy's exact mechanism is unknown. Peak incidence is in postadolescents, 10-15 years after diagnosis, and may involve up to 30% of people with IDDM.
    • Microalbuminuria is the first evidence of nephropathy. The exact definition varies slightly between nations but an increased AER is commonly defined as a ratio of first morning–void urinary albumin levels to creatinine levels that exceeds 10 mg/mmol, or as a timed overnight AER of more than 20 mcg/min but less than 200 mcg/min. Early microalbuminuria may resolve. Glomerular hyperfiltration occurs, as do abnormalities of the glomerular basement membrane and glomeruli.
    • In a patient with nephropathy, AER increases until frank proteinuria develops, and this may progress to renal failure. Blood pressure rises with increased AER, and hypertension accelerates the progression to renal failure.
    • Progression may be delayed or halted by improved diabetes control, by administration of angiotensin-converting enzyme inhibitors (ACE inhibitors), and by aggressive blood pressure control.
    • Regular urine screening for microalbuminuria provides opportunities for early identification and treatment to prevent renal failure.
  • A child younger than 15 years with persistent proteinuria may have a nondiabetic cause and should be referred to a pediatric nephrologist for further assessment.
  • Diabetic neuropathy affects both the peripheral and autonomic nerves. Hyperglycemic effects on axons and microvascular changes in endoneural capillaries are amongst the proposed mechanisms.
  • Autonomic changes involving cardiovascular control (eg, heart rate, postural responses) have been described in as many as 40% of children with diabetes. Cardiovascular control changes become more likely with increasing duration and worsening control.
  • In adults, peripheral neuropathy usually occurs as a distal sensory loss.
  • Macrovascular disease
  • While this complication is not seen in pediatric patients, it is a significant cause of morbidity and premature mortality in adults with diabetes.
  • People with IDDM have twice the risk of fatal myocardial infarction (MI) and stroke than people unaffected with diabetes; for women, the MI risk is 4 times greater. People with IDDM also have 4 times greater risk for atherosclerosis.
  • The combination of peripheral vascular disease and peripheral neuropathy can cause serious foot pathology.
  • Smoking, hypertension, hyperlipidemia, and poor diabetic control greatly increase the risk of vascular disease.
  • Associated autoimmune diseases are relatively common in children and include the following:
  • Hypothyroidism affects 2-5% of children with diabetes.
  • Hyperthyroidism affects 1% of children with diabetes; the condition is usually discovered at the time of diabetes diagnosis.
  • Although Addison disease is uncommon, affecting fewer than 1% of children with diabetes, it is a life-threatening condition that may reduce the insulin requirement and increase the frequency of hypoglycemia. (These effects may also be the result of unrecognized hypothyroidism.)
  • Celiac disease, associated with an abnormal sensitivity to gluten in wheat products, is probably a form of autoimmune disease and may occur in as many as 5% of children with IDDM.
  • Necrobiosis lipoidica is probably another form of autoimmune disease. This condition is usually, but not exclusively, found in patients with IDDM. Necrobiosis lipoidica affects 1-2% of children and may be more common in children with poor diabetic control.
  • Limited joint mobility, primarily affecting hands and feet, is believed to be associated with poor diabetic control.
  • Originally described in approximately 30% of patients with IDDM, limited joint mobility occurs in 50% of patients older than 10 years who have had diabetes longer than 5 years. The condition restricts joint extension, making it difficult to press the hands flat against each other. The skin of patients with severe joint involvement has a thickened and waxy appearance.
  • Limited joint mobility is associated with increased risks for diabetic retinopathy and nephropathy. Improved diabetes control over the past several years appears to have reduced the frequency of these additional complications by an approximate 4-fold factor. More recent patients also have markedly fewer severe joint mobility limitations.
  • Apart from severe DKA or hypoglycemia, IDDM has little immediate morbidity.
  • The risk of complications relates to diabetic control. With good management, patients can expect to lead full, normal, and healthy lives. Nevertheless, the average life expectancy of a child diagnosed with type 1 diabetes has been variously suggested to be reduced by 13-19 years, compared with their nondiabetic peers.
Patient Aducation
  • Education is a continuing process involving the child, family, and all members of the diabetes team.
Read more!
posted by Bunda at 15:14 | Permalink | 0 comments
Friday, 13 June 2008
What is Pre Diabetes?
A condition that raises persons risk of developing Type 2 diabetes,heart deseases and stroke.
before people develope type 2 diabetes,they almost always have "pre Diabetes"..Blood glucose level that are higher than normal but not yet high enough to be diagnosed as diabetes.
    -Pre Diabetes may have no sign and symptoms but may get dark patches of skin,usually on the back of neck,elbow,knees and armpit.(acantosis nigricans)
    -Fasting blood sugar Test
    Blood is drown after 8 hours fast to test the blood sugar.if Blood sugar level is 6.1 - 6.9mmol/l
    (impaired fasting glucose)
    -Family HIstory,having a parents or sibling with Diabetes,increase your chance to have type 2 diabetes
    -Inactivity,physical activity help to maintain ideal body weight as we know that obesity is risk faktor of type 2 diabetes
    -Gestational.if you have developed diabetes during pregnancy,or you gave a birth to a baby greater than 4 kilograms.
    -Obesity,being over weight increases fatty cells,this condition blocking the ability of the insulin to enter the body cell(insulin resistence)
    _Age,as we grow older the risk of type 2 diabetes increase due to inactivity,weight gain,and it is increasing among all ages groups
    -Ethnicity,it is not clear why some races are more likely to develop diabetes than other.

    • Diabetes currently affects 246 million people worldwide and is expected to affect 380 million by 2025.
    • In 2007, the five countries with the largest numbers of people with diabetes are India (40.9 million), China (39.8 million), the United States (19.2 million), Russia (9.6 million) and Germany (7.4 million).
    • In 2007, the five countries with the highest diabetes prevalence in the adult population are Nauru (30.7%), United Arab Emirates (19.5%), Saudi Arabia (16.7%), Bahrain(15.2%), and Kuwait (14.4%).
    • By 2025, the largest increases in diabetes prevalence will take place in developing countries.
    • Each year a further 7 million people develop diabetes.
    • Each year 3.8 million deaths are attributable to diabetes. An even greater number die from cardiovascular disease made worse by diabetes-related lipid disorders and hypertension.
    • Every 10 seconds a person dies from diabetes-related causes.
    • Every 10 seconds two people develop diabetes.
    • Diabetes is the fourth leading cause of global death by disease.
    • At least 50% of all people with diabetes are unaware of their condition. In some countries this figure may reach 80%.
    • Up to 80% of type 2 diabetes is preventable by adopting a healthy diet and increasing physical activity.
    • Diabetes is the largest cause of kidney failure in developed countries and is responsible for huge dialysis costs.
    • Type 2 diabetes has become the most frequent condition in people with kidney failure in countries of the Western world. The reported incidence varies between 30% and 40% in countries such as Germany and the USA.
    • 10% to 20% of people with diabetes die of renal failure.
    • It is estimated that more than 2.5 million people worldwide are affected by diabetic retinopathy.
    • Diabetic retinopathy is the leading cause of vision loss in adults of working age (20 to 65 years) in industrialized countries.
    • On average, people with type 2 diabetes will die 5-10 years before people without diabetes, mostly due to cardiovascular disease.
    • Cardiovascular disease is the major cause of death in diabetes, accounting for some 50% of all diabetes fatalities, and much disability.
    • People with type 2 diabetes are over twice as likely to have a heart attack or stroke as people who do not have diabetes. Indeed, people with type 2 diabetes are as likely to suffer a heart attack as people without diabetes who have already had a heart attack.
    Read more!
    posted by Bunda at 19:56 | Permalink | 0 comments
    Thursday, 5 June 2008
    As we know from beginning that pansreatic islets contain cell types as Alpha cell,Betha cell.Alpha cell producting gulcagon n beta cell producting Insulin.

    Insulin n glucagon are the 2 principal hormones controling Carbohidrate metabolism Insulin is powerfull Hypoglycemic agent while glucagon is a hyperglycemic agent.both of this hormones to maintain balance and normal blood glucose.


    Insulin is secreted by the beta cells of the pancreas in response to high blood sugar, although a low level of insulin is always secreted by the pancreas. After a meal, the amount of insulin secreted into the blood increases as the blood glucose rises. Likewise, as blood glucose falls, insulin secretion by the pancreatic islet beta cells decreases.

    In response to insulin, cells (muscle, red blood cells, and fat cells) take glucose in from the blood, which ultimately lowers the high blood glucose levels back to the normal range
    it goes through different stages of development.the end of stage is pro insulin which is insulin + c peptide

    What is The Action of Insulin?
    Insulin is vital for life,its is infortan for metabolism of
  • Carbohidrat(potato,rice)
  • Fat (butter,Oil)
  • Protein(fish,meat.chicken)

  • All this type of food are converted to glucose and used by the body as energy.
    If the body cell as a room so insulin as a key.to helps glucose to enter the body cell.
    Increases Insulin action starting
  • glucose uptake in muscle ,liver and adipose tissue
  • supresses glucose output from the liver.
  • increase formation of fat
  • Increase formation of protein

  • How Insulin Works?
    Insulin secreted at a low,base level(betwen meals).
    The blood glucose rises rapidly after the ingestion of glucose or(high carbohidrate meals)
    Insulin secretion stimulated to reduce the blood glucose level.(beta cell detect high blood glucose)
    High glucose concentration occures within the first hour and return to base level within 2 hours.


    Gucagon is secreted by the alpha cells of the pancreas when blood glucose is low. Blood glucose is low between meals and during exercise. When blood glucose is high, no glucagon is secreted from the alpha cells. Glucagon has the greatest effect on the liver although it affects many different cells in the body. Glucagon's function is to cause the liver to release stored glucose from its cells into the blood. Glucagon also the production of glucose by the liver out of building blocks obtained from other nutrients found in the body, for example, protein.

  • It is stumulated when blood glucose is very low.
  • Increases break down of glycogen to glucose in the liver n skeletal muscle.
  • increase break down of fat inti fatty acid in the adipose tissue
  • Increases syntethis and release of glucose in the liver(Gluconeogenesys).

  • Insulin signals a state of energy abundance, and activates glucose uptake, metabolism and storage as glycogen in muscle and fat tissue. These organs make up most of the body's mass. At the same time, insulin restrains processes that release stored energy; lipolysis and ketogenesis, glycogenolysis, proteolysis and gluconeogenesis. Insulin is necessary for uptake of amino acids to tissues and for protein synthesis. Insulin is THE central actor in homeostasis; the stabilization of the internal milieu.

    Insulin and glucagon act together to balance metabolism .In general we can say that insulin favors anabolic reactions; glucagon, catabolic reactions.

    Read more!
    posted by Bunda at 14:59 | Permalink | 0 comments
    Wednesday, 4 June 2008
    A fish -shaped graysh-pink nodular gland that stretches transversely across the posterior abdominal wall in the epigastric region that secretes various subtances such as digestives fluid,insulin and glucagon.
    The pancreas is an elongated, about 15cm long. The right side of the organ (called the head) is the widest part of the organ and lies in the curve of the duodenum (the first section of the small intestine). The tapered left side extends slightly upward (called the body of the pancreas) and ends near the spleen (called the tail).

    The pancreas is made up of two types of tissue:
  • Exocrine tissue
    The exocrine tissue secretes digestive enzymes. These enzymes are secreted into a network of ducts that join the main pancreatic duct, which runs the length of the pancreas Cluster of cells(acini) which secrete digestive enzymes into the duodenum via the pancreatic duct which unites to the common bile duct Liver,biliary system and exocrine they secrete enzymes which help the3 major types of food : fat,protein and carbohodrates. to be digested and store in the liver(Food is stored in the liver in simple form to be used as second fuel:
  • Fat stored-->fatty acid
  • protein stored -->Amino acid
  • CHO stored -->Glycogen Liver and Pancreatic Enzymes Liver secretes : bile and bile salts --> fat digestion Pancreas secretes
  • Amylase -->CHO digestion
  • Lipase -->Fat digestion
  • Trypsin -->protein digestion.
  • Endocrine tissue
    The endocrine tissue, which consists of the islets of Langerhans, secretes hormones into the bloodstream.

  • The human pancreas is an amazing organ with two main functions:
    1. To produce pancreatic endocrine hormones (e.g., insulin & glucagon) which help regulate many aspects of our metabolism and
    2. To produce pancreatic digestive enzymes.
    The hormone function of the pancreas is the emphasis of this portion of Endocrine Web ~ this is referred to as the Endocrine Pancreas. Pancreatic production of insulin, somatostatin, gastrin, and glucagon plays an important role in maintaining sugar and salt balance in our bodies and therefore any problem in the production or regulation of these hormones will manifest itself with problems with blood sugar and fluid / salt imbalances.

    Irregularly shaped patches of endocrine tissue in the pancreas. The normal human pancreas has about one million of them. Beta cells, the most common islet cells, produce insulin to regulate blood glucose. (Inadequate production of insulin is characteristic of diabetes mellitus.) Alpha cells produce an opposing hormone, glucagon, which releases glucose from the liver and fatty acids from fat tissue; these favour insulin release and inhibit glucagon secretion. Delta cells produce somatostatin, which inhibits somatotropin (a major pituitary hormone), insulin, and glucagon; its metabolic role is not clear. Small numbers of another type of cell secrete pancreatic polypeptide, which slows down nutrient absorption.

    Cell types :
    Hormones produced in the Islets of Langerhans are secreted directly into the blood flow by (at least) four different types of cells:

    Islets can influence each other through paracrine and autocrine communication, and beta-cells are coupled electrically to beta-cells (but not to other cell-types).

    Paracrine feedback
    The paracrine feedback system of the islets of Langerhans has the following structure:
    • Insulin: Activates beta cells and inhibits alpha cells.
    • Glucagon: Activates alpha which activates beta cells and delta cells.
    • Somatostatin: Inhibits alpha cells and beta cells
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    posted by Bunda at 14:52 | Permalink | 0 comments