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Diabetes Mellitus By Dr. Hanan Said A li PowerPoint Presentation
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Diabetes Mellitus By Dr. Hanan Said A li

Diabetes Mellitus By Dr. Hanan Said A li

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Diabetes Mellitus By Dr. Hanan Said A li

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  1. Diabetes Mellitus By Dr. Hanan Said Ali

  2. Objectives • Define diabetes mellitus. • Identify the aetiology and classification of diabetes mellitus. • Discuss the pathophysiology of diabetes mellitus • Enumerate the clinical manifestations . • Describe the management of diabetes mellitus. • Identify the complications of diabetes mellitus. • Describe the hypoglycaemia in DM

  3. Diabetes Mellitus Definition • A group of metabolic diseases characterized by hyperglycaemia resulting from defect in insulin secretion, insulin action or both. Aetiology and classification 1- Type 1 diabetes mellitus( previously termed insulin- dependent DM or Juvenile onset DM) 2- Type 2 diabetes mellitus ( previously termed noninsulin dependent DM or maturity – onset DM.

  4. Diabetes Mellitus Aetiology and classification 1- Type 1 diabetes mellitus It is characterized by: • Insulinopence ( insulin deficit) and dependent on exogenous insulin sustain life. • Onset before age 30, but may occur at any age. • Person’s body built is generally lean. • Variable rate of beta- cell destruction. • Clinical presentation is usually rapid (polyuria, polydipsia, polyphagia, weight loss.

  5. Diabetes Mellitus Aetiology and classification • 2- Type 2 diabetes mellitus • 90% of people with diabetes M. Have type 2 has strong genetic influences. • No requirement for exogenous insulin to sustain life at least initially. • Persons usually are obese. • Onset usually after 40

  6. Diabetes Mellitus - Pathophysiology • In absolute insulin deficiency , the pancreas produces either no insulin or very little. • In relative insulin deficiency the pancreas produces either normal or excessive amount of insulin, but the body is unable to use it effectively glucose level elevated. • When insulin is deficient relative to blood sugar level, led to  blood sugar

  7. Diabetes Mellitus - Pathophysiology • The body attempts to form its own usable glucose by protein catabolism and gluconecegenesis. This process lead to Hyperglycmia state. • Hyperglycemia creates Hyperosomolardiuresis in the kidneys  Water  electrolytes are lost in the urine due to lack or lose the battle to reabsorb the eltra fluid lead to polyurea.

  8. Diabetes Mellitus - Pathophysiology • Polydipsia (Excessive thirst)  to develops as the body initially tries to compensate for the fluid loss. • Polyphagia (Excessive eating)  Due to protein catabolism continue patients lose weight.

  9. Clinical Manifestations • When insulin deficiency occurs, glucose remains in the blood stream and produces an osmotic effect on intracellular and interstitial fluid • polyuria • Polydipsia ( thirst) • Without sufficient insulin, the patient may experience hunger hunger (polyphagia) as body turns to other energy resources besides glucose; first fat and then protein. • Visual blurring. Fatigue and weight loss. : :

  10. Management Diagnosis • Complete history and physical examination. • Blood test, including: • Fasting blood glucose. • Postprandial blood glucose. • Haemoglobin. • Cholesterol and triglyceride levels. • Blood urea nitrogen and serum creatinine, electrolytes

  11. Diagnosis • Urineincluding: • Complete urine analysis. • Microalbuminuria, Culture and sensitivity. • Glucose and acetone. • Funduscopic examination. • Neurologic examination. • Blood pressure. • Monitoring of weight. • Doppler scan

  12. Treatment of Type 1 DM • The treatment include the following: Insulin , diet and exercise. Common Insulin used for DM: • Quick- acting insulin , regular. • Intermediate acting insulin: NPH, Lente. • Combination insulin 70%NPH and 30% regular. Regular or quick- acting insulin requires that supplemental snack of 15 gram of carbohydrate be given to match the peak action of insulin

  13. Treatment of Type 2 DM • Oral hypoglycemic agents  This drug are not insulin but they stimulate the pancreatic islent to produce insulin and enhance cellular sensitivity to insulin. such as sulfonylureas. • Dietary control should be provided before starting oral agents.

  14. Management Principles of dietary teaching • Eat according to the prescribed meal plan: A dietary need related to the specific patient’s body weight, occupational age activities. • Learn to recognize, appropriate, food portions; can result in accurate portion allotments

  15. Management Principles of dietary teaching cont. • Never skip meals The body requires food at regularly-spaced intervals throughout the day. Omission or delay of meals can result hypoglycaemia.

  16. Management Exercise Benefits of exercises for the person with DM • Improves insulin sensitivity. • Lowers blood glucose during and after ex. • Improve lipid profile. • May improve some hypertension. • Assists with weight loss, preserve lean body mass. • Promote cardiovascular fitness. • Increase strength and flexibility and sense of well- being.

  17. Management Risks of exercises for the person with DM • Precipitation of cardiovascular disease. • Hypoglycaemia if taking insulin or oral- agents. • Hyperglycaemia after strenuous exercise. • Worsening of long- term complication • Proliferative retinopathy. • Peripheral neuropathy. • Autonomous neuropathy.

  18. Management Precautions for exercise • Take extra carbohydrates before exercise. • Check blood glucose before, during, afterward exercise. • Do not exercise in extreme heat or cold. • If glucose is over 250 mg/dl, check urine ketones; if negative, okay to exercise; if positive, take insulin; don't exercise until ketones are negative

  19. Precautions for exercise • Exercise should not cause shortness of breath and stopped with any onset of chest pain or dyspnea. • Inspect feet daily and after exercise. • Person with insensitive feet should choose good shoes for walking, avoid running. • Person with hypertension should avoid arms exercise.

  20. Complications of Diabetes Mellitus Acute complications include: 1. Hypoglycaemia . 2. Diabetes ketoacidosis (DKA) 3. Hyperglycaemic hyperosmalornonketonic coma (HHNC) Diabetes ketoacidosis (DKA) Diabetic coma may develop quickly or over several days or weeks.

  21. Diabetes ketoacidosis (DKA) Causes 1.Too little insulin accompanied by increased calorie intake. 2. Physical or emotional stress. 3. Inadequate treatment of existing DM. 4. Insulin is not taken as prescribed. 5. Infection. 6. Undiagnosed diabetes.

  22. Diabetes ketoacidosis (DKA) Assessment Finding Assessment Finding Eyes appear sunken. Breath orders of ketone. Rapid , weak pulse. Laboured breathing (kussmauls respiration) Fever Urinary frequencies. Glycosuria and knenouria. • Dry mouth • Thirst. • Abdominal pain • Nausea and vomiting • Gradually increasing restlessness, confusion, lethargy. • Flushed dry skin. • Serum glucose greater than 300mg/dl

  23. Diabetes ketoacidosis (DKA) Diagnostic Measures Blood glucose, CBC, Keton PH. Electrolytes, BUN, ABG, urine sp. Gr., PH sugar . Treatment 1. Low dose insulin IV infusion method. (5 to 10 units of insulin per hour in normal saline solution is administered until ketoacidosis is reversed)

  24. Diabetes ketoacidosis (DKA) Treatment Cont. When glucose level of 250 mg/dl is reached, a solution contain 5% dextrose in saline is given to prevent hypoglycaemia along with IV or SC insulin to maintain in blood glucose level

  25. Diabetes ketoacidosis (DKA) Nursing Management • Monitor vital signs, loc, cardiac rhythm, O2 saturation, urine output. • Assess breath sound for fluid overload. • Monitor serum glucose and serum K. • Administration of sodium bicarbonate with sever acidosis (PH lesser than 7-0).

  26. Chronic complications of diabetes • Micro vascular: • Diabetes retinopathy. • Diabetic nephropathy. • Neuropathy. • Painful peripheral neuropathy (Pain, loss of sensation to temperature, loss of deep tendon reflexes, muscle wasting and weakness).

  27. Chronic complications of diabetes • Amyotrophy ( Acute anterior thigh pain or numbness, weakness to hip flexion on examination . • Macro vascular : Dyslipidaemia , hypertension, coronary artery diseases,

  28. Hypoglycaemia in DM Definition • Hypoglycaemia or low blood glucose occurs when proportionately too much insulin is in the blood for the available glucose. Causes • Alcohol intake with food. • Too much exercise without compensation. • Too little food- delayed – omitted , inadequate intake.

  29. Hypoglycaemia in DM Causes Cont. • Diabetes medication or food taken at wrong time. • Loss of weight with change in medication. • A decrease in available blood glucose can results sympathetic nervous system activation and the release of epinephrine.

  30. Hypoglycaemia in DM Clinical Manifestations Clinical Manifestations Headache. Nervousness. Faintness, dizziness. Unsteady gait, slurred speech. Hunger. Change in vision. Seizures, coma. • Blood glucose less than 50 mg/dl. • Cold, clammy skin. • Numbness of fingers, toes, mouth. • Rapid heart beat. • Emotional changes.

  31. Hypoglycaemia in DM Treatment of Hypoglycaemia: • Immediate ingestion of 5- 20 gm of simple carbohydrates. • Ingestion of another 5- 20 gm of simple carbohydrates in 15 minutes if no response or relief. • Contacting of physician if no relief is obtained. • Discussion with physician with medication dosage.

  32. Hypoglycaemia in DM Preventing measure of hypoglycaemia: • Taking prescribed medications at proper time. • Accurate administration of insulin or oral agents. • Ingestion of all ordered diet foods at proper time. • Provision of compensation for exercise.

  33. Hypoglycaemia in DM Preventing measure of hypoglycaemia: • Ability to recognise and know symptoms and treat them immediately. • Carrying of simple carbohydrate (sugar). • Education of friends, family employees about symptoms and treatment. • Checking blood glucose as ordered.

  34. Hypoglycaemia in Non - DM • Hypoglycaemia in the nondiabetic person is characterised by subnormal plasma glucose, generally less than 50 mg/dl. • It may be asymptomatic, may cause adrenergic symptoms ( anxiety, irritability, palpitation , diaphoresis, and pallor) • Neurologlycopenic symptoms include (mental confusion, seizures, and coma)

  35. Hypoglycaemia in Non - DM Diagnosis • Appropriate signs and symptoms. • Appropriate abnormal blood glucose. • Responses to normalised blood glucose with carbohydrates ingestion.

  36. Hypoglycaemia in Non - DM Causes of fasting hypoglycaemia. • Insulin Excess • Exogenous insulin surreptitiously. • Insulin producing islets cell tumour. • Islets hyperplasia. 2. Increased hepatic glucose production • Advanced renal disease • Advanced liver disease

  37. Hypoglycaemia in Non - DM • Sever sepsis • Secure malnutrition 3. Counter regulatory hormone deficiency. Hypopituitarism. 4. Hypothyroidism 5. Non islets cell tumours. 6. Autoimmune disease, Antibodies that stimulate the receptor.

  38. Hypoglycaemia in Non - DM Reactive hypoglycaemia • Generally occurs 3 to 5 hours after meals related to either primary delay in insulin secretion or rapidly rising postprandial glucose related to rapid gastric emptying post gastric surgery. • Failure of the pancreas to keep pace with this rapidly rising postprandial glucose results in later insulin hypersecretion and hypoglycaemia.

  39. Hypoglycaemia in Non - DM Prevention of Reactive hypoglycaemia • Delaying the postprandial glucose rise through increased dietary fiber and the use of complex carbohydrates. • Enhancing insulin sensitivity through exercise and weight reduction towards desirable body weight.

  40. Thank You