Diabetes Mellitus. Raja Nursing Instructor. Acknowledgement: Badil 09/03/2016

Transcription

1 Diabetes Mellitus Raja Nursing Instructor 09/03/2016 Acknowledgement: Badil

2 Objective: Define Diabetes Mellitus (DM) & types of DM. Understand the pathophysiology of Type-I & II DM. List the clinical features of Type I-II DM. Describe the medical management of Type I-II DM.

3 Function of pancreas Alpha (Glucagon) Beta cells (Insulin) Insulin Stimulate uptake of glucose Converting glucose to glycogen Increasing the production of fat & protein

4 Diabetes Mellitus Diabetes mellitus is metabolic disorder of carbohydrate, protein, and fat characterized by elevated levels of glucose in the blood (hyperglycemia) resulting from defects in insulin secretion, insulin action, or both

5 Classification of Diabetes mellitus Type -1 Diabetes (IDDM) Type -2 Diabetes (NIDDM) Gestational diabetes mellitus Diabetes mellitus associated with other conditions or syndromes/ secondary diabetes mellitus

6 Type -1 Diabetes (IDDM) Type -1 (5% 10% of all diabetes) Type-1 Diabetes Mellitus is cased by destruction of beta cells by autoimmune process. It is thought that combined genetic, immunologic, and possibly environmental (e.g., viral) factors contribute to beta cell destruction. Virus are rubella, mumps, Coxsackievirus etc.. DR3 and DR4 deficiency

7 Conti If the concentration of glucose in the blood exceeds the renal threshold for glucose, usually 180 to 200 mg/dl (9.9 to 11.1 mmol/l). The kidneys may not reabsorb all of the filtered glucose; the glucose then appears in the urine (glucosuria). When excess glucose is excreted in the urine, it is accompanied by excessive loss of fluids and electrolytes. This is called osmotic diuresis.

8 Conti Insulin normally inhibits glycogenolysis (breakdown of stored glucose) and gluconeogenesis. Due to insulin deficiency the gluconeogenesis process occurs that cause the fat breakdown. The end product of fat breakdown is ketone. Excessive ketones cause the DKA ( Diabetes Ketoacidosis)

9 Ketone Ketone bodies are acids that disturb the acid base balance of the body when they accumulate in excessive amounts. The resulting DKA may cause signs and symptoms such as abdominal pain, nausea, vomiting, hyperventilation, a fruity breath odor, and, if left untreated, altered level of consciousness, coma, and death.

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11 Conti Initiation of insulin treatment, along with fluid and electrolytes needed, is essential to treat hyperglycemia and DKA and rapidly improves the metabolic abnormalities.

12 Clinical characteristics and implications Onset any age, but usually young (<20 yrs) Usually thin at diagnosis Recent weight loss Etiology includes genetic, immunologic, or environmental factors (e.g., virus). Often have islet cell antibodies Little or no endogenous insulin Need insulin to preserve life Ketosis-prone when insulin absent Acute complication of hyperglycemia: diabetic ketoacidosis

13 Type -2 Diabetes Mellitus The two main problems related to insulin in type 2 diabetes are insulin resistance and impaired insulin secretion. Insulin resistance refers to a decreased tissue sensitivity to insulin. Normally, insulin binds to special receptors on cell surfaces and initiates a series of reactions involved in glucose metabolism.

14 Conti The exact mechanisms that lead to insulin resistance and impaired insulin secretion in type 2 diabetes are unknown.

15 Characteristics and Implications Type- 2 90% 95% of all diabetes: Obese 80% of type 2 Non-obese 20% of type 2 Onset any age, usually over 30 years Usually obese at diagnosis Causes include obesity, heredity.

16 Conti No islet cell antibodies Decrease in endogenous insulin, or increased with insulin resistance Most patients can control blood glucose through weight loss if obese. Oral antidiabetic agents may improve blood glucose levels if dietary modification and exercise are unsuccessful.

17 Clinical features Three Ps Ps : Polyphagia,Polyuria and Polydipsia Fatigue and weakness, sudden vision changes tingling or numbness in hands or feet, dry skin, skin lesions wounds that are slow to heal Recurrent infections.

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19 Investigations Fasting Plasma glucose levels exceeding 126 mg/dl Random plasma glucose levels exceeding 140 mg/dl HbA1C (A1C) 4% to 7% is normal

20 Diabetic management There are five components of diabetes management Nutritional management Exercise Blood glucose Monitoring Pharmacologic therapy Education

21 Diabetes treatment Oral anti-diabetic agents may be effective for patients who have type 2 diabetes that cannot be treated by diet and exercise alone. Anti-Diabetic medications Oral hypoglycemic agents Sulfonylureas Thiazolidinediones Biguanides Alpha-glucosidase inhibitors Insulins

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24 Metformin (Glucophage) Oral Antidiabetic Agents Biguanides Biguanides reduce hepatic glucose output It does not cause weight gain Metformin is usually the first-line medication used for treatment of type 2 diabetes It is generally prescribed at initial diagnosis in conjunction with exercise and weight loss Initial dosing is 500 mg once daily, then if need be increased to 500 mg twice daily up to 1000 mg twice daily

25 Sulfonylureas First widely used oral anti-hyperglycaemic medications They are insulin secretagogues, triggering insulin release The "second-generation" drugs are now more commonly used They are more effective than first-generation drugs and have fewer side effects All may cause weight gain

26 Conti The primary side effect is hypoglycemia They can not be used with type I diabetes, or diabetes of pregnancy They can be safely used with metformin or glitazones

27 First-generation agents Tolbutamide (Orinase) Acetohexamide (Dymelor) Tolazamide (Tolinase) Chlorpropamide (Diabinese)

28 Second-generation agents Glipizide (Glucotrol) Glyburide (Diabeta, Micronase, Glynase) Glimepiride (Amaryl) Gliclazide (Diamicron)

29 Thiazolidinediones Increase cellular sensitivity to insulin Pioglitazone (Actos) Rosiglitazone (Avandia)

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31 Rapid acting insulin Lispro (Humolog, Novolog Aspart) Onset of action minutes [may come on in 5 minutes ] Peak of action 1-2 hours Duration 3 4 hours

32 Short acting insulin Regular (clear so can be given IV) Onset of action 0.5 to 1 hour Peak of action 2 4 hours Duration of action 6 8 hours

33 Intermediate acting insulin NPH, Lente (chemicals added. Cloudy) Onset of action 1 4 hours Peak of action 4 12 hours Duration of action hours

34 Long acting insulin Ultralente Onset of action 4 8 hours Peak of action 18 hours Duration of action hours

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36 Reference Abrams, A. C. (1998). Clinical drug therapy: Rationales for nursing practice( 5 th ed.). New York: Lippincott. Joseph F, Smith. (2003). Antidiabetic drugs. Retrieved December 23, 2004 From http// Endocrine tumors of pancreas. (2003). Retrieved December 5, 2004 From Insulin Aspart. (2003). Retrieved December 6, 2004 From McCuistion, L. E, & Gutierrez, K.J.(2002). Real world nursing survival guide: Pharmacology. London: Suanders. (pp ) Antidiabetic drugs.(22 april,2004). Retrieved April,2005. From Aschenbrenner, D.S, Cleveland, L.W., & Venable, S.J. (2002). Drug therapy in nursing. New York: Lippincott.