Diabetes mellitus


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Diabetes mellitus

  2. 2. DiabetesMellitus  Chronic metabolic disorder  Body cannot metabolise fats, carbohydrates, and proteins because of a lack of, or ineffective use of the hormone insulin  classified into three primary types that are different disease entities but share the symptoms and complications of hyperglycemia (high blood glucose)
  3. 3. DiabetesMellitus  Type I Diabetes Mellitus:  Previously “Insulin Dependent Diabetes Mellitus” (IDDM)  Or Juvenile-Onset Diabetes  Type II Diabetes Mellitus:  Previously “Non-Insulin Dependent Diabetes Mellitus” (NIDDM)  Or Adult-Onset Diabetes  Gestational Diabetes Mellitus:  Or GDM
  4. 4. NormalCarbohydrateMetabolism andInsulinAction  Following the consumption of food, carbohydrates are broken down into glucose molecules in the gut  Glucose is absorbed into the bloodstream elevating blood glucose levels  This rise in glycaemia stimulates the secretion of insulin from the beta cells of the pancreas  Insulin is needed by most cells to allow glucose entry
  5. 5. NormalCarbohydrateMetabolism andInsulinAction  Insulin binds to specific cellular receptors and facilitates entry of glucose into the cell, which uses the glucose for energy  The increased insulin secretion from the pancreas and the subsequent cellular utilization of glucose results in lowered of blood glucose levels  Lower glucose levels then result in decreased insulin secretion
  6. 6. NormalCarbohydrateMetabolism andInsulinAction  Following meals, the amount of glucose available from carbohydrate breakdown often exceeds the cellular need for glucose  Excess glucose is stored in the liver in the form of glycogen, which serves as a ready reservoir for future use  When energy is required, glycogen stores in the liver are converted into glucose via glycogenolysis, elevating blood glucose levels and providing the needed cellular energy source
  7. 7. NormalCarbohydrateMetabolism andInsulinAction  The liver also produces glucose from fat (fatty acids) and proteins (amino acids) through the process of gluconeogenesis  Glycogenolysis and gluconeogenesis both serve to increase blood glucose levels Thus, glycaemia is controlled by a complex interaction between the gastrointestinal tract, the pancreas, and the liver
  8. 8. TheRoleof Insulinin hyperglycaemiaandhypoglycaemia  If insulin production and secretion are altered by disease, blood glucose dynamics will also change  If insulin production is decreased, glucose entry into cells will be inhibited, resulting in hyperglycaemia  The same effect will be seen if insulin is secreted from the pancreas but is not used properly by target cells  If insulin secretion is increased, blood glucose levels may become very low (hypoglycaemia) as large amounts of glucose enter tissue cells and little remains in the bloodstream.
  9. 9. TypeI DiabetesMellitus  Beta cells of pancreas are destroyed or suppressed  Subdivided into idiopathic and immune- mediated types
  10. 10. TypeI DiabetesMellitus  Onset is usually abrupt, before 30 years of age but may be diagnosed at any age  Type I Diabetics are usually of normal weight, or may be thin in stature  Since the pancreas produces absolutely no insulin, the patient must rely on exogenous insulin, administered for survival  Patients are highly susceptible to diabetic ketoacidosis
  11. 11. TypeI DiabetesMellitus PathophysiologyofIdiopathicDiabetesMellitus  With idiopathic type, patients have a permanent insulin deficiency with no evidence of autoimmunity  Often lack antibodies found in immune- mediated type 1 diabetes  May be able to go without insulin therapy for some periods of time
  12. 12. TypeI DiabetesMellitus PathophysiologyofImmune-MediatedDiabetes  Occurs when there is autoimmune destruction in which the body secretes substances that attack and destroy the beta cells in the islets of Langerhans within the pancreas  This attack causes an inflammatory response in the pancreas called insulitis, ceasing insulin production  One or more key antibodies are found in 85- 90% of people with this form of type 1 diabetes
  13. 13. DiabeticKetoacidosis(DKA)  Inadequate insulin hinders glucose uptake by fat and muscle cells  Glucose accumulates in blood  Liver responds to demands of energy starved cells by converting glycogen to glucose, further increasing blood glucose levels  When glucose levels exceed renal threshold, excess excreted in urine  Insulin-deprived cells respond by rapid metabolism of proteins
  14. 14. DiabeticKetoacidosis(DKA)  Results in loss of intracellular potassium and phosphorus and excessive liberation of amino acids  Liver converts these acids into urea and glucose  Blood glucose levels grossly elevated  Results in increased serum osmolarity and glucosuria, leading to massive fluid loss from osmotic diuresis causing fluid and electrolyte imbalances
  15. 15. DiabeticKetoacidosis(DKA)  Water loss excedes glucose and electrolyte loss, contributing to hyperosmolarity  This perpetuates dehydration, decreasing the glomerular filtration rate and reducing amount of glucose excreted in urine DEADLY CYCLE: Diminished glucose excretion  raises blood glucose levels  hyperosmolarity and dehydration  SHOCK  COMA  DEATH
  16. 16. DiabeticKetoacidosis(DKA)  SIMULTANEOUSLY – Absolute insulin deficiency causes cells to convert fats into glycerol and fatty acids for energy  Fatty acids can’t be metabolised as quickly as released, so accumulate in liver  Converted to ketones (ketoacids)  Ketones accumulate in blood and urine (acidosis)  Acidosis leads to more tissue breakdown  More ketosis  More acidosis  Eventually SHOCK  COMA  DEATH
  17. 17. TypeII DiabetesMellitus  Caused by:  Resistance to insulin action in target tissues  Abnormal insulin secretion  Inappropriate hepatic gluconeogenesis (over production of glucose)  Consequence of obesity and sedentary lifestyle
  18. 18. TypeII DiabetesMellitus Pathophysiology  Problems arise when insufficient insulin produced or body (fat, muscle or liver) cells resist insulin  When body cells develop a resistance to insulin, there is a difficulty with glucose entering cells  As a result, cells don’t get enough energy  Lack of energy causes glucose to build up in the blood vessels  Can result in damage to body organs especially if poorly managed
  19. 19. GestationalDiabetesMellitus  Gestational diabetes mellitus (GDM) is defined as glucose intolerance of variable degree with onset or first recognition during pregnancy  The placental hormones – oestrogen, placental lactogen , glucagon and cortisol interfere with insulin receptors making the woman temporarily diabetic  Usually develops in the second or third trimester
  20. 20. GestationalDiabetesMellitus  Risk factors for gestational diabetes include:  Advanced maternal age (>30 years)  Ethnicity (Maori, Pacific Islander, Indian, Chinese)  Obesity (Prepregnancy BMI >30 – dependent on ethnicity)  Obstetrical history of diabetes , unexplained still birth or neonatal death or macrosomia  Strong family history of diabetes  Glucosuria on two separate occassions in current pregnancy  Multiple pregnancy
  21. 21. DiabetesinPregnancy  Pregnancy characterised by several factors that produce a diabetogenic state  Insulin and carbohydrate metabolism is altered in order to make glucose more readily available to the fetus  Women with DM do not have the capacity to increase insulin secretion in response to the altered carbohydrate metabolism in pregnancy  Glucose therefore accumulates in the maternal and fetal system, leading to significant morbidity and mortality
  22. 22. SignsandSymptoms  Polyuria and polydipsia: Polyuria is due to osmotic diuresis secondary to hyperglycemia. Thirst is due to the hyperosmolar state and dehydration  Polyphagia with weight loss or muscle wasting:The weight loss with a normal or increased appetite is due to depletion of water and a catabolic state with reduced glycogen, proteins, and triglycerides
  23. 23. SignsandSymptoms  Fatigue and weakness:This may be due to muscle wasting from the catabolic state of insulin deficiency, hypovolemia, and hypokalemia  Nocturnal enuresis (bed-wetting): Severe enuresis secondary to polyuria can be an indication of onset of diabetes in young children
  24. 24. SignsandSymptoms  Blurred vision:This also is due to the effect of the hyperosmolar state on the lens and vitreous humor. Glucose and its metabolites cause dilation of the lens, altering its normal focal length  Muscle cramps:This is due to electrolyte imbalance
  25. 25. SignsandSymptoms  Gastrointestinal symptoms: Nausea, abdominal discomfort or pain, and change in bowel movements may accompany acute DKA. Acute fatty liver may lead to distention of the hepatic capsule, causing right upper quadrant pain. Persistent abdominal pain may indicate another serious abdominal cause of DKA, eg, pancreatitis. Chronic gastrointestinal symptoms in the later stage of diabetes are due to visceral autonomic neuropathy
  26. 26. SignsandSymptoms  Peripheral neuropathy:This presents as numbness and tingling in both hands and feet, in a glove and stocking pattern. It is bilateral, symmetric, and ascending neuropathy, which results from many factors, including the accumulation of sorbitol in peripheral sensory nerves due to sustained hyperglycemia
  27. 27. SignsandSymptoms Symptoms at the time of the first clinical presentation can usually be traced back several days to several weeks; however, beta cell destruction may have started months, or even years, before the onset of clinical symptoms
  28. 28. FetalComplications  Miscarriage  In women with pre-existing diabetes, there is a 9- 14% risk of miscarriage  Supoptimal glycaemic control and advanced diabetes also posses a significant risk
  29. 29. FetalComplications  Birth Defects  With DM the risk of structural abnormality is increased to 5-10% (normally 1-2%)with poor glycaemic control prior to conception  Two-thirds of anomalies affect the cardiovascular and nervous systems  Neural tube defects occur 13-20 times more frequently in diabetic women  Genitourinary, gastrointestinal, and skeletal anomalies are also more common  Because birth defects occur during the critical 3-6 weeks after conception, nutritional and metabolic intervention must be initiated well before pregnancy begins
  30. 30. FetalComplications  Fetal Growth Restriction  IUGR occurs significantly in pregnancy where women have pre-existingType 1 DM  The most important 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
  31. 31. FetalComplications  Fetal Growth Acceleration  Caused by excessive body fat stores, stimulated by excessive glucose delivery during diabetic pregnancy  Approximately 30% of fetuses of women with diabetes mellitus in pregnancy are large for gestational age (LGA). In pre-existing 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
  32. 32. FetalComplications  Fetal Obesity  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  Macrosomia is typically defined as a birthweight above the 90th percentile for gestational age or greater than 4000 grams  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
  33. 33. FetalComplications  Metabolic Syndrome  Glucose intolerance and higher serum insulin levels are more frequent in children of diabetic mothers as compared to normal controls  The childhood metabolic syndrome includes childhood obesity, hypertension, dyslipidemia, and glucose intolerance  Fetuses of diabetic women that are born large for gestational age appear to be at the greatest risk
  34. 34. FetalComplications  BirthTrauma  Injuries of birth, including shoulder dystocia and brachial plexus trauma, are more common among infants of diabetic mothers  Common birth injuries associated with diabetes are brachial plexus, facial nerve injury, and cephalohematoma
  35. 35. FetalComplications  Polycythaemia  Hyperglycemia is a powerful stimulus to fetal erythropoietin production mediated by decreased fetal oxygen tension  Hypoglycaemia  Aproximately 15-25% of neonates delivered from women with diabetes during gestation develop hypoglycemia during the immediate newborn period  Unrecognized postnatal hypoglycemia may lead to neonatal seizures, coma, and brain damage
  36. 36. FetalComplications  Hyperbilirubinaemia  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
  37. 37. FetalComplications  Respiratory Problems  The majority of the literature indicates a significant biochemical and physiological delay in infants of diabetic mothers  Fetal lung maturity is thought to occur later in pregnancies with poor glycaemic control regardless of class of diabetes
  38. 38. MaternalComplications  Diabetic Retinopathy  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  Studies show that while half the women with pre- existing retinopathy experienced deterioration during pregnancy, all the patients had partial regression following delivery and returned to their prepregnant state by 6 months postpartum  Rapid induction of glycaemic control in early pregnancy stimulates retinal vascular proliferation
  39. 39. MaternalComplications  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  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
  40. 40. MaternalComplications  Chronic Hypertension  Complicates approximately 1 in 10 diabetic pregnancies overall  Patients with underlying renal or retinal vascular disease are at a substantially higher risk  Patients with chronic hypertension and diabetes are at increased risk of intrauterine growth restriction, superimposed preeclampsia, abruptio placentae, and maternal stroke
  41. 41. MaternalComplications  Pre-Eclampsia  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 and pregravid body mass index
  42. 42. TestsandInvestigations HbA1c  HbA1c is a test that measures the amount of glycosylated hemoglobin in blood  Glycosylated hemoglobin is a molecule in red blood cells that attaches to glucose (blood sugar)  Elevated levels of glycosylated hemoglobin if there more glucose in the blood  The test gives a good estimate of how well diabetes is being managed over the last 2 or 3 months (life of erythrocyte)  No preparation or fasting required prior
  43. 43. TestsandInvestigations HbA1c  Results  An elevated HbA1c increases the risk of complications such as retinopathy, nephropathy, neuropathy, heart disease, and stroke  Especially true if HbA1c remains high for a long period of time  HbA1c normally 3-6%  Abnormal results mean that blood glucose levels have not been well-regulated over a period of weeks to months  If HbA1c is above 7%, it means diabetes is poorly controlled
  44. 44. TestsandInvestigations Polycose  Woman without known diabetes should be offered routine screening for GDM  Test is a non fasting 1 hour 50g glucose challenge test, preferably in morning  One hour later, blood is taken  Performed at 24-28 weeks of pregnancy  Women need written and full information about this so they can make an informed choice
  45. 45. TestsandInvestigations Polycose  Results  If result is >7.8 mmol/L  GTT  If result is 7.2 – 7.7 mmol/L  Rescreen 2 weeks later if known risk factors for GDM  If result is <7.8 mmol/L but known risk factors are present  Offer rescreening or GTT to assess whether glucose tolerance deteriorating
  46. 46. TestsandInvestigations GlucoseToleranceTest  Test is a fasting 75g glucose tolerance test  Blood is taken: - Prior to test - 1 hour after glucose load - 2 hours after glucose load  Usual diet in days prior to the test  Fast for 12 hours prior to the test  Repeat if clinically indicated, even though first GTT has been normal
  47. 47. TestsandInvestigations GlucoseToleranceTest  Results  Gestational Diabetes Mellitus confirmed if:  Fasting glucose: 5.5 mmol/L or greater  2 hour glucose: 9.0 mmol/L or greater
  48. 48. Section88 MaternityNotice ReferralGuidelines  LEVEL 3 (Code 1019) - Pre-existing DM Insulin Dependent or Non Insulin Dependent  LEVEL 2 (Code 1020) - GDM well controlled on diet  LEVEL 3 (Code 1021) - GDM requiring Insulin Consideration of ‘Shared Care’ or intrapartum midwifery care may be an option for women with GDM
  49. 49. Section88 MaternityNotice ReferralGuidelines  LEVEL 3 (Code 8044) - Infant of a Diabetic Mother with any abnormal findings e.g.  Hypoglycaemia  Poor feeding  Macrosomia
  50. 50. Management Pre-PregnancyCareforType1or2DM  Assessment is made of current diabetic control, aiming for pre-meal glucose of <6 mmol/L and HbA1c of ≤7%  Insulin dosage reviewed  Women withType 2 DM on oral hypoglycaemics will need to transfer to insulin to prevent possibility of teratogenesis  Higher-dose folic acid supplementation  Smoking cessation support is arranged  Assessment and management is provided for diabetes complications
  51. 51. Management Pre-ExistingDiabetesMellitus  Booking visit – care recommendations and options  Ideally should be seen in a combined clinic by a team that includes a physician, obstetrician, specialist diabetes nurse, specialist midwife and dietician  Seen as often as required in order to maintain good diabetic control and undertake relevant screening  Blood glucose levels should be monitored frequently (4-8x per day using reflective meter) and insulin levels adjusted accordingly  Additional estimations of blood glucose control, such as monthly HbA1c measurements recommended  Diet high in fibre beneficial as carbohydrates released slowly and therefore more constant BSL can be achieved
  52. 52. Management Pre-ExistingDiabetesMellitus  Advise women on early recognition of the signs and symptoms of urinary and vaginal infections  Anomaly ultrasound should be offered at 20 weeks gestation, and consider fetal echocardiography at 20-22 weeks to detect cardiac abnormalities  Serum screening for Down Syndrome is altered with maternal diabetes and care should be taken when interpreting results  A baseline measurement of the fetal AC should be taken at 20 weeks gestation, followed by serial measurements every 2-4 weeks commencing at 24 weeks to detect IUGR, macrosomia and polyhydramnios  See in daily assessment unit if problems or on wards if inpatient
  53. 53. Management GestationalDiabetesMellitus  After screening and confirmation, referral according to Section 88 Guidelines  Educate women regarding complications of uncontrolled blood glucose levels on her health and her baby’s  Partake in 3-way discussion as MultidisciplinaryTeam member  Good communication with women regarding scope and with other professionals regarding care  Refer if Blood glucose levels high/unstable  Be aware of local protocols  Continue to support, educate, offer continuity of care eg. for postnatal care, etc
  54. 54. Medications Insulin  NovoRapid  Insulin aspart, whereby its molecules enable the uptake of glucose into cells by binding onto receptor sites and concurrently preventing the release of glucose from the liver  Dosage is based on the needs of the patient when reviewed by the physician and facilitates a quick onset of action when comparing it to human insulin, and a shorter duration of action after subcutaneous injection  Unlike glucose however, insulin does not cross the placental barrier
  55. 55. Medications Insulin  Protaphane  Similar to NovoRapid  Is an isophane insulin suspension and its actions are equal to that of human insulin  One significant difference is that its time of onset is 1.5 hours, longer than NovoRapid and long acting, lasting for up to 24 hours  Again, the dose is patient-dependent, and determined by the physician in accordance with the needs of the patient
  56. 56. Medications Metformin  Metformin is a biguanide by-product, which produces an antihyperglycaemic effect where there is insulin secretion from the pancreas, although the action of the drug is not fully understood  It is suggested that it may mimic or improve the effects of insulin on peripheral receptor sites, and that this increased sensitivity appears to be a result of an increase in the amount of insulin receptor sites on the cell surface  Other proposed mechanisms of action include glucogenesis inhibition within the liver or a delay in the absorption of glucose from the gastrointestinal tract  In pregnancy metformin does cross the placenta, however there is no research to indicate that metformin is teratogenic