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Diabetes Mellitus


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Diabetes Mellitus, medical and nursing management with its Complecations

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Diabetes Mellitus

  1. 1. DIABETES MELLITUS Ms. Amandeep Kaur MMCON
  2. 2. INTRODUCTION Type 2 diabetes is sometimes called a “life style” disease as it more common in people who don’t do enough exercise, have an unhealthy diet and obese. Type 2 Diabetes was previously seen mainly in older adults, however it is becoming more common in young children due to obesity and overweight children.
  3. 3. HISTORY The Indian physician Sushruta in the 6th century B.C. noticed the sweet nature of urine in such patients and termed the condition MADHUMEHA.
  4. 4. Diabetes Mellitus Greek word "diabainein" meaning "to siphon or pass through" Latin word "mellitus" meaning "sweetened with honey" "To pass through sweetened with Honey"
  5. 5. DIABETIC MELLITUS DEFINITION:- Diabetes is a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both.
  6. 6. EPIDEMIOLOGY Globally 382 million people had diabetes in 2013 By 2035, this number will rise to 592 million In India 65.1 million people had diabetes in 2013 By 2035, this number will increase by 70.6%
  7. 7. Courtesy: 2015 International Diabetes Federation Epidemiology
  8. 8. ANATOMY OF PANCREAS  The adult pancreas is a transversely oriented retroperitoneal organ extending from the "C " loop of the duodenum to the hilum of the spleen EXOCRINEsecretion  pancreatic juice enzymes promote the digestion of carbohydrates, proteins and fats ENDOCRINE secretion  Insulin and glucagon- enter portal vein – transported directly to the liver – regulate metabolism of carbohydrates, proteins and fats.
  9. 9. PANCREAS  15- 20% α cells synthesize and secrete GLUCAGON  70- 80% β cells synthesize and secrete INSULIN  1-8% δ cells synthesize and secrete STOMATOSTATIN and GASTRIN  1-2% F- cells secrete PANCREATIC POLYPEPTIDE which decreases the absorption of food from the GIT
  10. 10. INSULIN  Polypeptide hormone produced by β- cells of islets of Langerhans of pancreas  Insulin is a protein made of 2 chains- alpha and beta  Anabolic hormone STRUCTURE OF INSULIN
  11. 11. REGULATION OF INSULIN SECRETION  Factors stimulating insulin secretion : Glucose: The effect is more predominant when glucose is administered orally. Arise in blood glucose level is a signal for insulin secretion. amino acids: gastrointestinal hormones: Gastrointestinal hormones (secretin, gastrin) enhance the secretion of insulin.
  12. 12. REGULATION OF INSULIN SECRETION  Factors inhibiting insulin secretion • Epinephrine is the most potent inhibitor of insulin release. • In emergency situations like stress, extreme exercise and trauma, the nervous system stimulates adrenal medulla to release epinephrine. • Epinephrine suppresses insulin release and promotes energy metabolism by Mobilizing energy-yielding compounds- glucose from liver and fatty acids from adipose tissue
  13. 13. TERMINOLOGY Gluconeogenesis : The synthesis of glucose from non- carbohydrate precursors( e.g. amino acids, glycerol) Glycogenesis: The formation of glycogen from glucose. Glycogenolysis : The breakdown of glycogen to glucose
  14. 14. ACTIONS OF INSULIN Stimulation of the activity of glycolytic enzymes Reduces the activity of the enzymes of gluconeogenesis Increased synthesis of glycogen Increased uptake of of glucose by resting skeletal muscles Reduction of blood glucose level Reduction of lipolysis and stimulation of lipid synthesis
  15. 15. INSULIN  Pancreas secretes 40-50 units of insulin daily in two steps: • Secreted at low levels during fasting ( basal insulin Secretion. • Increased levels after eating (prandial). • An early burst of insulin occurs within 10 minutes of Eating. • Then proceeds with increasing release as long as hyperglycemia is present.
  16. 16. CLASSIFICATION  Classification by American diabetic association 2009 : • Type 1 diabetes • Type 2 diabetes • Gestational diabetes mellitus (GDM) • Secondary DM: Hormonal problems, pancreatic disorders, drugs
  17. 17. TYPE 1 DM  Juvenile / IDDM(5 to 10%)  Autoimmune destruction of pancreatic beta cells.  Individual has an absolute insulin deficiency and no longer produces insulin.  Such patients are absolutely dependent on exogenously administered insulin for survival.
  19. 19. TYPE 2 DM  Most common type.  Comprises 90 to 95% of DM cases.  Most type 2 DM patients are overweight, and most are diagnosed as adults.  Approximately half of the patients are unaware of their disease.
  20. 20. Peripheral resistance to insulin, especially in muscle cells Increased production of glucose by the liver Insulin secretary defect of the beta cells • Obesity contributes greatly to insulin resistance. • Insulin resistance generally decreases with weight loss. TYPE 2 DM The underlying pathophysiologic defect in type 2 DM is characterized by the following three disorders:
  21. 21. COMPONENTS OF DM-II Type 2 Diabetes Insulin Resistance B-cell Dysfunction
  22. 22. RISK FACTORS  NON-MODIFIABLE:  Age: 45 or more  Race : African American, Asian American, Hispanic or Latino.  Familial history : a parent, or siblings with diabetes.
  23. 23. RISK FACTORS  MODIFIABLE: Pre diabetes Heart and blood disease Hypertension Low HDL cholesterol and high triglycerides. Obesity Polycystic ovary syndrome Physical inactivity
  24. 24. CLINICAL PRESENTATION Patients can be asymptomatic  Polyuria.  Polydipsia.  Polyphagia.  Fatigue.  Weight loss.  Most patients are discovered while performing urine glucose screening.
  25. 25. DIAGNOSIS  Fasting Plasma Glucose  Oral Glucose Tolerance Test (OGTT)  Glycoselated Hemoglobin (HbA1c)  Urinalysis • Glycosuria • Ketone bodies
  26. 26. HBA1C •Measures the amount of glycated haemoglobin in blood.•HbA1c is not sensitive enough to detect DM but is standard for the long term monitoring. the gold
  27. 27. ADDITIONAL INVESTIGATIONS;  Lipid profile  Fundoscopic examination  LFT ,  Urine analysis  ECG  Test to assess other complications
  28. 28. Any one test should be confirmed with a second test, most often fasting plasma glucose (FPG). DIAGNOSTIC CRITERIA • Classic signs of HYPERGLYSEMIA with CPG ≥200mg/ • OGTT ≥200mg/dL • FPG ≥126mg/dL • A1C ≥ 6.5%
  29. 29. CONDITION 2 HRS GLUCOSE FASTING GLUCOS E HbA1C UNIT Mg/dl Mg/dl % Normal <140 <110 <6 Impaired fasting glycemia <140 110 – 126 6 -6.4 Impaired glucose tolerance >140 <126 6 – 6.4 DM >200 >126 > 6.5
  31. 31. The major components of the treatment of diabetes are: MANAGEMENT OF DM • Medical Nutrition Therapy(Diet and Exercise)A • Oral hypoglycaemic therapyB • InsulinC
  32. 32.  Dietary treatment should aim at: Ensuring weight control. Providing nutritional requirements. Allowing good glycaemic control with blood glucose levels as close to normal as possible. Correcting any associated blood lipid abnormalities. A. DIET
  33. 33. DIETARY MANAGEMENT DIETARY MANAGEMENT Follow individualized meal plan and snacks as scheduled diet based on pts. wt., age, occupation and activity. Balanced diabetic diet – 50% CHO, 30% fats, 20% CHON(Co2, H2o, O2, Nitrogen), vitamins and minerals. Meal should include more fiber and starch and fewer simple or refined sugars.
  34. 34. DIETARY MANAGEMENT  If taking insulin, eat extra food before periods of vigorous exercise.  Routine blood glucose testing before each meal and at bedtime is necessary during initial control, during illness and in unstable pts.  Excessive salt intake is to be avoided. It should be particularly restricted in people with hypertension and those with nephropathy.
  35. 35.  Eat grains in the least processed state possible.  Limit potatoes and refined grain products.  Avoid concentrated sweets (jellies, jams, cakes, ice cream).  Choose foods with healthy fats.  Have 3 meals and one or two snacks each day.  Eat slowly and stop when full.  Avoid periods of fasting and feasting, Do not skip meals. How to eat low Glycemic Index food
  36. 36.  Physical activity promotes weight reduction and improves insulin sensitivity, thus lowering blood glucose levels.  Exercise same time and duration of day.  People should, however, be educated about the potential risk of hypoglycaemia and how to avoid it.  Avoid during poor metabolic control.  Avoid trauma to extremities. EXERCISE
  37. 37. EXERCISE PRECAUTIONS  Patients who have BS >200mg/dl and who have urine ketones should not begin exercise until urine tests are NEGATIVE.  Use of proper footwear.  Avoid exercise in extreme heat or cold.  Have snacks after the exercise , to avoid post exercise hypoglycemia.
  38. 38.  There are currently four classes of oral anti-diabetic agents: i. Biguanides ii.Insulin Secretagogues – Sulphonylureas iii.Insulin Secretagogues – Non-sulphonylureas iv.α-glucosidase inhibitors v.Thiazolidinediones (TZDs) vi.DPP4i B. ORAL ANTI-DIABETIC AGENTS
  39. 39. Oral Anti-diabetic Agents
  40. 40. BIGUANIDES  Metformin : is the only drug of this class presently available in market  It does not cause hypoglycaemia  MOA : They increase glucose uptake and utilisation in skeletal muscle (thereby reducing insulin resistance) and reduce hepatic glucose production (gluconeogenesis).  Pharmacokinetic : Metformin has a half-life of about 3 hours and is excreted unchanged in the urine.
  41. 41. METFORMIN  Side effects : -Dose-related gastrointestinal disturbances -lactic acidosis is a rare but potentially fatal toxic effect -Long-term use may interfere with absorption of vitamin B12  Contra indications: Renal failure Hepatic disease Heart failure or shock.
  42. 42. INSULIN SECRETAGOGUES SULFONYLUREAS : Inhibit KATP Channel of ß-cells First-generation agents Tolbutamide Acetohexamide Tolazamide Chlorpropamide Second-generation Glipizide Glyburide Glimepiride
  43. 43. SULFONYLUREAS  Hypoglycemia is the most common and most serious adverse event associated with SU therapy.  Weight gain, regarded as a class effect of Su’s  Contraindicaton: liver failure, renal failure patients.  Most sulfonylureas cross the placenta and enter breast milk; as a result, use of sulfonylureas is contraindicated in pregnancy and in breast feeding.
  44. 44. NON-SULFONYLUREA SECRETAGOGUES  MEGLITINIDES • MOA: Inhibit KATP Channel of ß-cells • Very fast onset of action, rapidly metabolized by liver enzymes, with a peak effect within 1 hour, the duration of action is 5–8 hr. • Short duration of action and a low risk of hypoglycaemia • Medications in this Class: Repaglinide, Nateglinide.
  45. 45. THIAZOLIDINEDIONES  ↓ Insulin resistance by making muscle and adipose cells more sensitive to insulin. They also suppress hepatic glucose production.  Side effects: weight gain, oedema, Hypoglycemia (if taken with insulin)  Contraindication: patients with abnormal LFT or CHF  Medications in this class: Pioglitazone, Rosiglitazone,
  46. 46. Α-GLUCOSIDASE INHIBITORS  Acarbose : An inhibitor of intestinal α-glucosidase.  MOA : It delays carbohydrate absorption, reducing the postprandial increase in blood glucose .  Unwanted effects : flatulence, loose stools or diarrhoea, and abdominal pain and bloating.  Like metformin, it is helpful in obese type 2 patients, and it can be co-administered with Metformin.
  47. 47. TREATMENT OF TYPE 2 DIABETES Diagnosis Therapeutic Lifestyle Change Combination Therapy - Oral Drug with Insulin Combination Therapy - Oral Drugs Only Monotherapy
  48. 48.  If glycaemic control is not achieved (HbA1c > 6.5%) with lifestyle modification within 1 –3 months, ORAL ANTI-DIABETIC AGENT should be initiated.  In the presence of marked hyperglycaemia in newly diagnosed symptomatic type 2 diabetes (HbA1c > 8%, FPG > 11.1 mmol/L), oral anti- diabetic agents can be considered at the outset together with lifestyle modification. MONOTHERAPY
  49. 49. Combination oral agents is indicated in: Newly diagnosed symptomatic patients with HbA1c >10 Patients who are not reaching targets after 3 months on monotherapy COMBINATION ORAL AGENTS
  51. 51. Short-term use:  Acute illness, surgery, stress and emergencies  Pregnancy  Breast-feeding  Insulin may be used as initial therapy in type 2 diabetes  Severe metabolic decompensation (diabetic ketoacidosis, hyperosmolar nonketotic coma, lactic acidosis, severe hypertriglyceridaemia). INSULIN THERAPY
  52. 52. Long-term use:  If targets have not been reached after optimal dose of combination therapy, consider change to multi-dose insulin therapy. INSULIN THERAPY
  54. 54. ROUTES OF ADMINISTRATION  Subcutaneous for long term regular use  Intravenous infusion in acute conditions- diabetes Ketoacidosis, Perioperative period, Hyperosmolar Nonketotic state ONLY NEUTRAL/ CLEAR INSULIN CAN BE USED  Intraperitoneal – Peritoneal dialysis patients  Inhaled insulin- experimental
  55. 55. COMPLICATIONS OF INSULIN THERAPY Hypoglycemia Lipodystrophy Systemic allergic reactions Insulin resistence
  56. 56. METHODS OF INSULIN THERAPY 1. Insulin syringe: 2. Insulin pens 3. Jet injectors 4. Insulin Pumps
  57. 57. PATIENT EDUCATION  Taking care of diabetes will help to reduce blood glucose, blood pressure, and cholesterol levels in target ranges.  Caring for your diabetes can also help prevent other health problems over the years. Follow your healthy eating plan every day. Be physically active every day. Take medicines every day. Check blood glucose levels every day.
  59. 59. COMPLICATIONS OF DIABETES MELLITUS I. Acute complications: diabetic ketoacidosis hypoglycemia diabetic nonketotic hyperosmolar coma II. Chronic complications:  A. Microvascular Retinopathy Nephropathy Neuropathy Diabetic Foot Dermopathy b. Macrovascular Cerbro-vascular. Cardio-vascular. Peripheral Vascular Disease.
  60. 60. HYPOGLYCEMIA  Hypoglycemia is the most frequent acute complication in diabetes.  Signs and symptoms are most common when blood glucose levels fall <60 mg/dL.  CAUSE: Missing meals or excessive exercise Alterations or errors in insulin dosage. Alcohol ingestion.
  61. 61. CLINICAL MANIFESTATIONS OF HYPOGLYCEMIA:  Autonomic dysfunctions: 1. Hunger 2. Tremor 3. Palpitation 4. Anxiety 5. Pallor 6. Sweating Neurologic dysfunctions: 1.Impaired thinking 2.Change of mood 3.Irritability 4.Headache 5.Convulsion 6.Coma
  62. 62. MANAGEMENT  MILD (Self treated) Oral fast acting carbohydrate (10- 15gm) – taken as glucose drink or candy  Severe :(semi conscious or comatose patient) IV hypertonic glucose 25% or 50% concentration Glucagons injection- i.m Glucagon (1mg)
  63. 63. DIABETIC KETOACIDOSIS - It is a true emergency - CAUSES: Omitting insulin in type 1 DM or increase insulin requirements, Infection Trauma Myocardial Infarction Stroke Surgery Emotional stress  Mortality rate is around 5%.
  65. 65. MANAGEMENT  Fluid replacement: 0.9% Na.  Insulin therapy for hyperglycemia: To restore the metabolic abnormalities. Titrate the dose according to the blood glucose level. • 50U insulin in 50 ml NS iv via infusion pump 6U/hr initially 3U/hr when blood glucose < 270mg/dl 2U/hr when blood glucose < 180mg/dl  Electrolyte correction.  Acidosis correction.  Treatment of precipitating cause.
  66. 66. HYPERGLYCEMIA HYPEROSMOLAR NONKETONIC SYNDROME (HHNK)  Occurs when there is insufficient insulin to prevent hyperglycemia, but there is enough insulin to prevent Ketoacidosis.  Occurs in all types of diabetes, Esp Diabetes Type 2.  Life threatening medical emergency.  Characterized by :  Plasma osmolarity 340 mOsm/L or greater normal: 280 -300).  Blood glucose severely elevated, 600 - 1000 or 2000 (normal 70- 110).  Undetectable ketonuria and Absence of acidosis.
  67. 67. HHNKS  Major difference from diabetic ketoacidosis is the lack of ketonuria because there is some residual ability to secrete insulin in NIDDM. CLINICAL MANIFESTATION:  Altered level of consciousness (lethargy to coma)  Neurological deficits: hyperthermia, motor and sensory impairment, seizures  Dehydration: dry skin and mucous membranes, extreme thirst.
  68. 68. MACRO-VASCULAR COMPLICATIONS  Ischemic heart diseases.  Cerebrovascular diseases.  Peripheral vascular diseases. Diabetic patients have a 2 to 6 times higher risk for development of these complications than the general population
  69. 69. HYPERTENSION IN DM  Mostly present at diagnosis  Affects about 60% of patients  Secondary to insulin resistance  Increases risk for retinopathy, nephropathy  Dyslipidaemia in DM  Most common abnormality is  HDL and  Triglycerides  A low HDL is the most constant predictor of Cardiovascular disease in DM.
  70. 70. PERIPHERAL VASCULAR DISEASE  Increased risk for Types 1 and 2 diabetics.  Development of arterial occlusion and thrombosis resulting in gangrene.  Gangrene from diabetes is themost common cause of non- traumatic lower limb amputation.
  71. 71. SCREENING FOR MACROVASCULAR COMPLICATIONS 1. Examine pulses for cardiovascular diseases. 2. Lipid profile. 3. ECG. 4. Blood pressure.
  72. 72.  Microvascular complications are specific to longstanding hyperglycaemia.  Both Type1 DM and Type2 DM are susceptible to microvascular complications.  The duration of diabetes and the quality of diabetic control are important determinants of microvascular abnormalities. MICROVASCULAR COMPLICATIONS
  73. 73. DIABETIC RETINOPATHY  Affects 60 % of Type 2 diabetics  progressive, irreversible vision loss. Cotton wool spots  Damage to the tiny blood vessels that supply the eye • Micro aneurysms • Scattered exudates • Cotton wool spots (<5) • Venous dilatations NORMAL RETINA
  74. 74. DIABETIC NEPHROPATHY (DN) Diabetic nephropathy is defined by persistent albuminuria (>300 mg/day), decrease glomerular filtration rate and rising blood pressure. About 20 – 30% of patients with diabetes develop diabetic nephropathy - Manifested as: - Microalbuminuria - Progressive diabetic nephropathy leading to end- stage renal disease
  75. 75. TREATMENT TO PREVENT PROGRESSION TO DN  All diabetic patients should be screened annually for microalbuminurea.  Tight glycemic control and management of the blood pressure  ACE-inhibitors are recommended to decrease the progression of nephropathy  Smoking cessation.  Proteins restriction.  Lipid reduction.
  76. 76. DIABETIC NEUROPATHY  Damage to the Nerves due to hyperglycemia  Typses of Neuropathies… Sensory-Motor Polyneuropathy • Numbness, paresthesias. • Feet are mostly affected, hands are seldom affected. • Complicated by ulceration (painless), charcot arthropathy • Decreased deep tendon reflexes
  77. 77. DIABETIC NEUROPATHY Autonomic neuropathy  Can affect almost any system - Manifested by orthostatic hypotension, diabetic diarrhea, erectile dysfunction, and difficulty in urination.
  79. 79. NURSING ASSESSMENT Obtain history : it includes, Current problems and General health history Family history Has the patient experienced polyuria, polydipsia, polyphagia, and any other symptoms? Number of years since diagnosis of DM? Symptoms of complications?
  80. 80. NURSING ASSESSMENT PHYSICAL EXAMINATION:  General: Recent wt. loss or gain, fatigue, anxiety  Skin: lesion, infections, dehydration,  Eyes: changes in vision, “floaters, halos, cataracts…  Cardiovascular: orthostatic hypotension, claudication  GI: diarrhea, increased hunger and thirst  GU: polyurea, nocturia  Neurologic: numbness, and tingling of extremities
  81. 81. 1.Imbalanced nutrition : more than body requirement related to intake of excess of activity expenditures. Assess the current timings and content of meals Advise patient on the importance of an individualized meal plan in meeting weight loss goals. Explain the importance of exercise in maintain / reducing body weight. Assist the patient to establish goals for weekly weight loss and incentives to assist in achieving them.
  82. 82. 2. Risk for injury ( hypoglycemia) related to effects of insulin, inability to eat. Closely monitor blood glucose levels to detect hypoglycemia. Instruct the patient in the importance of accuracy in insulin preparation and meal timings to avoid hypoglycemia. Treat hypoglycemia promptly with 15 to 20 gm of fast acting carbohydrates. Encourage patients to carry sugar candy all times. Encourage patient to wear identification bracelet
  83. 83. 3. Deficit knowledge related to use of oral hypoglycemic agents. Assess level of knowledge of disease and ability to care self. Assess adherence to diet therapy, monitoring procedures, medication, treatment, and exercise regimen. Assess for signs for hyperglycemia or hypoglycemia. Perform skin and extremity assessment for peripheral neuropathy or any injury in feet and lower extremities.
  84. 84. 4. Risk for impaired skin integrity related to decreased sensation and circulation to lower extremities. Assess feet and legs for skin temperature sensation, soft tissue injures, corn, dryness, hammer toe, Maintain skin integrity by protecting feet from break down. Use heel protectors, special mattresses, foot cradles for patient on bed rest. Avoid Appling drying agent to skin. (alcohol) Apply moisturizers to maintain suppleness and prevent cracking and fissures. Instruct patient in foot care guidelines
  85. 85. FOOT CARE Patient should Check feet daily Wash feet daily Keep toe nails short Protect feet Always wear shoes Look inside shoes before putting them on Always wear socks Break in new shoes gradually
  86. 86. 5. Ineffective coping related to chronic disease and complex self care regimen. Discuss with the patient the perceived effect of diabetes on lifestyle, finances, family life, occupation. Explore previous coping strategies and skills that have had positive effects. Encourage patient and family participation in DM self care regimen. Assist family in providing emotional support.
  87. 87. SPECIAL PATIENT POPULATION 1. Adolescent Type 2 DM - Type 2 DM is increasing in adolescent. - Lifestyle modification is essential in these patients. - If lifestyle modification alone is not effective, metformin the only labeled oral agent for use in children (10-16 years).
  88. 88. CONCLUSION Type 2 diabetes is a “life style” disease, characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both. Caring for diabetes can also help prevent other health problems over the years.