diabetes mellitus presentation

overview presentation of diabetes mellitus for students

1. DIABETES MELLITUS

2. OBJECTIVES At the end of presentation the learner's would be able to; Define diabetes mellitus. Difference between type l, type ll and gestational diabetes mellitus. Describe the Pathophysiology of type l and type ll diabetes mellitus. Discuss the diagnosis of diabetes mellitus. Explain the treatment and prevention of diabetes mellitus. Enlist the complication of diabetes mellitus.

3. DIABETES MELLITUS Diabetes mellitus is a disorder of carbohydrate metabolism characterized by high level of blood glucose resulting from impaired ability to produce insulin, insulin action or both.

4. TYPES OF DIABETES MELLITUS There are three main types of diabetes mellitus; Type l diabetes or insulin dependant diabetes Type ll diabetes or non insulin dependant diabetes Gestational diabetes

5. TYPE I DIABETES MELLITUS Type I diabetes also known as juvenile or insulin-dependant diabetes. It is an autoimmune condition in which the pancrease produce little or no insulin due to body attacking its own pancrease with antibodies and destroy the beta cell. Age mostly occur 4 to 7 years and 10 to 14 years.

6. PATHOPHYSIOLOGY Type l diabetic is idiopathic and autoimmune Organ-specific deficit may induce an autoimmune attack on beta cell s. this attack, in turn, causes an inflammatory response in the pancrease called insulitis. Islet cell antibodies may be present long before symptoms become apparent. These immune markers also precede evidence o f beta cell deficiency. Autoantibodies against insulin have also been noted. By the time the disease become apparent, 80% of the beta cells are gone.

7. CAUSES OF TYPE I DIABETES The exact cause is unknown. Genetic predisposition Faulty beta cells in the pancrease Exposure to virus and other environmental factor RISK FACTORS Genetic Family history Geography Age mostly 4 to 14 years

8. SIGN AND SYMPTOMS Polydipsia or Increase thirst Polyuria or Frequent urination Polyphagia or Extreme hunger Weight loss Blurred vision Fatigue and weakness Irritability and mood change

9. TREATMENT AND PREVENTION One of the best treatment of type I diabetes is insulin; short acting – insulin ( Humulin R) Long acting insulin (novolog, flexpen, fiasp). Intermediate –acting –insulin ( H umulin-n) Long-acting insulin ( lantus, levemir) According to researcher Type I diabetes is not preventable right now but can be prevented by taking good care of your body –maintaining healthy diet and staying physically fit and active.

10. TYPE II DIABETES Type ll diabetes also known as adult-onset diabetes or non- insulin dependant diabetes characterized by high blood glucose level, insulin resistance and lack of insulin. In type ll diabetes the beta cell of the pancrease produce insulin but the body is unable to use it effectively because the cell of the body are resistance to the action of insulin.

11. PATHOPHYSIOLOGY

12. RISK FACTORS MODIFIABLE RISK FACTORS Obesity Sedentary life style Hypertension Stress factors Smoking NON MODIFIABLE RISK FACTORS Ethnicity Family history of type ll diabetes Age Gender History of gestational diabetes inflammation

13. SIGN AND SYMPTOMS Polydipsia or increase thirst Polyuria or increase urination Polyphagia or extreme hunger Weight loss Slow-healing sores Areas of darkened skin, usually in the arms and neck.

14. TREATMENT Metformin (BIGUANIDES- Glucophage) should be the first line drug for managing type ll diabetes. Insulin and sulfonylureas (Glipizide-Glucotrol, glyburide- D iabeta, Glimepiride-Amaryl) should be second line. Thiazolidinediones (Piogiltazones-Actos) should be third line drug for managing type ll diabetes.

15. Gestational diabetes Gestational diabetes develop s during pregnancy. Gestational diabetes is c aused when the insulin receptor do not function properly. This is likely due to pregnancy related factor such as the presence of human placental lactogen that interference with susceptible insulin receptor. Mostly detected at 24 to 28 weeks of pregnancy. Gestational diabetes goes away after birth but increase risk of developing type 2 D M for mother and children.

16. RISK FACTORS AND SYMPTOMS RISK FACTORS Body mass index more than 30/kg/m2 Previous gestational diabetes Family history of diabetes Previous baby weight 4.5kg or more Sedentary life style History of smoking SIGN AND SYMPTOMS Drinking a lot or polydipsia Urination more than usual Infection in bladder, vagina and skin The tummy looks bigger Nausea Vomiting Fatigue

17. DIAGNOSTIC EVALUATION Diabetes can be diagnosed in any of the following ways; History Physical examination Labs test

18. LABS DIAGNOSIS FBS (Fasting blood sugar) greater than or equal to 126 mg/dl. RBS (Random blood sugar) greater than or equal to 200mg/dl OGTT (Oral glucose tolerance test) more than or equal to 200 mg/dl, on the 2hours sample. HBA1C (Glycated Hemoglobin A1C) 6..1 to 7 target range for diabetes.

19. HISTORY Have you had increase thirst, increase urination and fatigue? How long have the symptoms been present? Have you had an increase in appetite? Have you lost weight lately? Is there a family history of diabetes? What other medical condition do you have? What are medicine are you currently taking? Have you been ill recently? Has growth and development progressed normally ( if the person is child)?

20. PHYSICAL EXAMINATION Assess skin for dehydration, infection and poor wound healing. Numbness and tingling of the extremities, tremor, twitching, drowsiness, lethargy and crying. Eyes; blurred vision, retinopathy, cataract, glaucoma. Cardiovascular; weak pulse, orthostatic hypotension, tachycardia, ECG changes. Respiratory ; breathing pattern, characteristics of metabolic acidosis Gastrointestinal; nausea, vomiting, abdominal bloating and diarrhea. Genitourinary; nocturia, and polyuria. Nutrition level; check weight and body mass index(BMI)

21. complication ACUTE COMPLICATION CHRONIC COMPLICATIION Hypoglycemia Diabetic ketoacidosis (DKK) Hyperosmolar hyperglycemic nonketotic syndrome(HHNS) Macrovascular-(atherosclerosis plaque) Coronary arteries- MI Cerebral arteries- stroke Peripheral vessels- ulcer, amputation, infection Microvascular (capillary damage) Retinopathy Neuropathy Nephropathy

22. Nursing intervention Monitor patient's FBS, RBS and HBA1C. Assess for sign of hyperglycemia such as polyphagia, polyuria, polydipsia, blurred vision. Assess for sign of hypoglycemia such as anxiety, tremor and slurring of speech, dizziness, diaphrosis. Assess feet for pulses, temperature , sensation and instruct the patient to avoid heating pads and always to wear shoes when walking. Teach the patient about role of exercise in diabetes. Teach patient about an importance of proper meal and adequate calorie intake. Teach the patient about disease process and problem associated with disease. Teach the patient how to administered insulin properly.

23. REFFRENCES Pathophysiology made incredible easy book 2 nd edition. American diabetes association guideline.