Diabetes mellitus type 2

Diabetes mellitus type 2, nursing prespective

1. DIABETES MELLITUS TYPE 2 PRESENTER: Esther Mary Mathew M.Sc Nursing 1 st year MODERATOR : Ms. Ujjwal Dahiya Lecturer, CON AIIMS .

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. History The earliest known record of diabetes was written on 3rd Dynasty Egyptian papyrus by physician ‘ Hesy -Ra’. He stated recurring urination as a sign of this illness

4. 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 .

5. "to pass through sweetened with honey"

6. DIABETIC MELLITUS Diabetes is a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both. 

7. 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%

8. Courtesy: 2015 International Diabetes Federation Epidemiology

9. 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 EXOCRINE secretion 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.

10. 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

11. 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

12. Regulation of insulin secretion Factors stimulating insulin secretion : Glucose: The effect is more predominant w hen 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.

13. 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

14. Actions of insulin

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. Glucose homeostasis

17. Classification Classification by American diabetic association 2009 : Type 1 diabetes Type 2 diabetes Gestational diabetes mellitus (GDM) Secondary DM: Hormonal problems, pancreatic disorders, drugs

18. 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. Type 2 diabetes mellitus

20. 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

21. 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 :

22. COMPONENTS OF DM-II Type 2 diabetes Insulin resistance  -cell dysfunction

23. Risk Factors NON-MODIFIABLE: Age: 45 or more Race : African American, Asian American, Hispanic or Latino. Familial history : a parent, or siblings with diabetes.

24. Risk Factors MODIFIABLE: Pre diabetes Heart and blood disease Hypertension Low HDL cholesterol and high triglycerides. Obesity Polycystic ovary syndrome Physical inactivity

25. RESEARCH INPUT High Bone Mineral Density and Fracture Risk in Type 2 Diabetes as Skeletal Complications of Inadequate Glucose Control. Ling Oei , Abbas , Karol Estrada et al Journal : Diabetes Care 2013 Jun; 36(6) Objective : To examine the influence of glucose control on skeletal complications.

26. RESEARCH INPUT RESEARCH DESIGN AND METHODS: prospective population-based study 420 participants with type 2 diabetes were classified by glucose control - according to HbA 1c adequately controlled diabetes (ACD:  n  = 203; HbA 1c  <7.5%) inadequately controlled diabetes (ICD;  n  = 217; HbA 1c ≥7.5%) no diabetes ( n  = 3,715)

27. RESEARCH INPUT RESULTS  : The ICD group had 1.1–5.6% higher BMD, and 1.2 to −1.8% narrower femoral necks than ACD and ND, respectively. Participants with ICD had 47–62% higher fracture risk than individuals without diabetes whereas those with ACD had a risk similar to those without diabetes. CONCLUSIONS  : Poor glycemic control in type 2 diabetes is associated with fracture risk.

28. Clinical Presentation Patients can be asymptomatic Polyuria Polydipsia Polyphagia Fatigue Weight loss Most patients are discovered while performing urine glucose screening

29. DIAGNOSIS Fasting Plasma Glucose Oral Glucose Tolerance Test (OGTT) Glycoselated Hemoglobin (HbA1c) Urinalysis Glycosuria Ketone bodies

30. HbA1c Measures the amount of glycated haemoglobin in blood. HbA1c is not sensitive enough to detect DM but is the gold standard for the long term monitoring.

31. Additional investigations; Lipid profile Fundoscopic examination LFT , Urine analysis ECG Test to assess other complications  

32. 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/Dl OGTT ≥200mg/ dL FPG ≥126mg/ dL A1C ≥ 6.5%

33. “WHO” diagnostic Criteria CONDITION 2 HRS GLUCOSE FASTING GLUCOSE 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

34. MANAGEMENT OF DIABETES MELLITUS

35. The major components of the treatment of diabetes are: Management of DM

36. 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

37. DIETARY MANAGEMENT DIETARY MANAGEMENT Follow individualized meal plan and snacks as scheduled Balanced diabetic diet – 50% CHO, 30% fats, 20% CHON, vitamins and minerals diet based on pts. size, wt., age, occupation and activity. Meal should include more fiber and starch and fewer simple or refined sugars.

38. 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

39. 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 GI food

40. 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

41. Exercise precautions Patients who have BS >250mg/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.

42. 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

43. Major Classes Body to insulin +/- control hepatic glucose production Stimulate the pancreas to make more insulin Slow the absorption of starches Thiazolidinediones Biguanides Sulfonylureas Meglitinides Alpha- glucosidase inhibitors

44. Oral Anti-diabetic Agents

45. 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.

46. 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 B 12 Contra indications: Renal failure Hepatic disease Hypoxic pulmonary disease Heart failure or shock Temporarily discontinued before any radiographic procedure involving intravenous iodinated contrast, as patients are at an increased risk of lactic acidosis .

47. Insulin Secretagogues SULFONYLUREAS : Inhibit K ATP Channel of ß-cells First-generation agents Tolbutamide Acetohexamide Tolazamide Chlorpropamide Second-generation Glipizide Glyburide Glimepiride

48. 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 P’kinetics : Orally given, Some is oxidised in the liver to moderately active products and is excreted in urine; 50% is excreted unchanged in the faeces.

49. 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

50. 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 ,

51. 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 .

52. Treatment of Type 2 Diabetes Diagnosis Therapeutic Lifestyle Change Combination Therapy - Oral Drug with Insulin Combination Therapy - Oral Drugs Only Monotherapy

53. 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

54. 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

55. DIABETES MANAGEMENT ALGORITHM

56. 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

57. Long-term use: If targets have not been reached after optimal dose of combination therapy, consider change to multi-dose insulin therapy. Insulin Therapy

58. INSULIN INJECTION SITES

59. 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

60. Complications of Insulin Therapy Hypoglycemia Lipodystrophy Systemic allergic reactions Insulin resistence Dawn phenomenon Somagyi's phenomenon

61. Methods of insulin therapy Insulin syringe: Insulin pens Jet injectors Insulin Pumps

62. 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 your medicines every day. Check your blood glucose levels every day.

63. COMPLICATIONS OF DIABETES

64. 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 .

65. 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

66. 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

67. 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)

68. 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%.

69. Clinical presentation

70. MANAGEMENT Fluid replacement: 0.9% NaCl IV 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.

71. 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

72. 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.

73. 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

74. 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.

75. 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

76. Screening for Macrovascular Complications 1. Examine pulses for cardiovascular diseases. 2. Lipid profile. 3. ECG. 4. Blood pressure.

77. 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 m icrovascular abnormalities. MICROVASCULAR C OMPLICATIONS

78. Diabetic retinopathy Affects 60 % of Type 2 diabetics progressive, irreversible vision loss. Damage to the tiny blood vessels that supply the eye Micro aneurysms Scattered exudates Cotton wool spots (<5) Venous dilatations NORMAL RETINA Cotton wool spots

79. Diabetic Nephropathy (DN) Diabetic nephropathy is defined by persistent albuminuria (>300 mg/day), decrease glom erular 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

80. 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.

81. Diabetic Neuropathy Damage to the Nerves due to hyperglycemia Types 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

82. Diabetic Neuropathy Autonomic neuropathy Can affect almost any system Manifested by orthostatic hypotension, diabetic diarrhea, erectile dysfunction, and difficulty in urination.

83. RESEARCH INPUT Effect of mechanical vibration on transcutaneous oxygen levels in the feet of type 2 diabetes mellitus patients.   Núñez Carrera L,  Alessi Montero A ,et al Journal of clinical medicine:  2016 Nov 18. objective : To determine whether whole body vibration favors some parameters of interest related to complications associated with the diabetic foot syndrome.( Transcutaneous oxygen levels (TcPO 2 )>40mmHg in cases of diabetic foot syndrome are associated with a good prognosis in the resolution of ulcers.)

84. METHOD: 54 patients with DM were included in a 12-week exercise program based on whole body vibration. Glycemic control was determined on the basis of the patients' levels of (HbA 1c ); sensitivity and TcPO 2  levels of each foot were also recorded. RESULTS: A significant 7mmHg increase was observed in the concentration of TcPO 2 . CONCLUSION: Whole body vibration may increase TcPO 2  levels with useful implications for the prevention or management of complications associated with restricted blood perfusion in the diabetic foot syndrome.

85. NURSING MANAGEMENT

86. 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?

87. 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

88. 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.

89. 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

90. 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. Deficit knowledge related to use of oral hypoglycemic agents

91. 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 Risk for impaired skin integrity related to decreased sensation and circulation to lower extremities.

92. 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

93. 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. Ineffective coping related to chronic disease and complex self care regimen.

94. 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)

95. 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.