diabetes mellitus & their complications


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diabetes mellitus & their complications

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  2. 2. PRESENTED BY : 09Z31R0003 09Z31R0005 09Z31R0028 09Z31R0033 09Z31R0039 G.VANI M.Pharm,Pharmacology GUIDED BY: Mrs. 2
  3. 3.  Introduction To Diabetes Mellitus Epidemiology Blue Circle Types Of Diabetes Mellitus Pathophysiology Clinical Manifestations Of Diabetes Mellitus Diagnosis Of Diabetes Mellitus Management Of Diabetes Mellitus Complications Of Diabetes Mellitus 3
  5. 5. Diabetes mellitus is a group of metabolic diseases in which a person has high blood sugar, either because the pancreas does not produce enough insulin or because cells do not respond to the insulin that is produced. This high blood sugar produces the classical symptoms of polyuria (frequent urination), polydipsia (increased thirst) and polyphagia (increased hunger). 5
  6. 6. EPIDEMIOLOGY About 16 million have diabetes. Around the world, the prevalence of diabetes is expected to double between 1994 and 2010, at which time about 240 million people will have the disease. The incidence of diabetes rises as the population ages and as the prevalence of obesity increases. Unfortunately, about half of those with diabetes are presently unaware that they have the disease. Most dental practices have a significant number of diabetic patients in their population. Based on data, an "average" practice would have between 60 and 70 diabetic individuals for every 1,000 patients, and 30 to 35 of these patients would be undiagnosed. 6
  7. 7. Continue……. Gestational diabetes occurs during pregnancy and usually resolves after delivery. Other types of diabetes may occur in individuals with certain genetic disorders, pancreatic diseases, infections, injuries to the pancreas, and endocrine diseases. Drug therapy with certain agents may also induce a diabetic state. 7
  8. 8. WORLD DIABETES DAY World Diabetes Day commemorates the global awareness campaign, which is held on NOV 14. It was introduced in 1991 by the International diabetes federation and the world health organization...In response to the alarming rise of diabetes around the world. The day also marks the birthday of FREDERICKBANTING who, along with CHARLES BEST, first conceived the idea to the discovery of insulin in 1922. 8
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  11. 11. Type 1 diabetes is an autoimmune destruction of pancreatic beta cells. Hence the individual has an absolute insulin deficiency and no longer produces insulin. Autoimmune beta cell destruction is thought to be triggered by an environmental event, such as a viral infection. Most type 1 diabetic individuals are of normal weight or are thin in stature. Since the pancreas no longer produces insulin, a type 1 diabetes patient is absolutely dependent on exogenously administered insulin for survivalwith type 1 diabetes are highly susceptible to diabetic People ketoacidosis. 11
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  13. 13. Most type 2 diabetes patients are overweight, and most are diagnosed as adults. The genetic influence in type 2 diabetes is greater than that seen with type 1. In addition to genetic influences, acquired risk factors for type 2 diabetes include obesity, advancing age, and an inactive lifestyle. pathophysiologic defect in type 2 diabetes does not involve autoimmune beta-cell destruction. Type 2 diabetes is characterized by the following three disorders: (1) peripheral resistance to insulin, especially in muscle cells; (2) increased production of glucose by the liver (3) altered pancreatic insulin secretion TYPE 2 DIABETIC PATIENTS OFTEN HAVE A GROUP OF DISORDERS THAT HAS BEEN CALLED "INSULIN RESISTANCE SYNDROME" OR SYNDROME X. 13
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  15. 15. It usually develops during the third trimester and significantly increases  The proper diagnosis and management of gestational diabetes improves pregnancy outcomes. As with type 2 diabetes, the pathophysiology of gestational diabetes is associated with increased insulin resistance.  Most patients with gestational diabetes return to a normoglycemic state after parturition; however, about 30 to 50% of women with a history of gestational diabetes will develop type 2 diabetes within 10 years. 15
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  17. 17. Pathophysiology of diabetes rests upon of the basics of carbohydrate metabolism and insulin action. consumption of food, carbohydrates are broken down into glucose molecules in the gut. Glucose is absorbed into the bloodstream elevating blood glucose levels. This rise in glycemia stimulates the secretion of insulin from the beta cells of the pancreas Insulin is needed by most cells to allow glucose entry. Insulin binds to specific cellular receptors and facilitates entry of glucose into the cell, which uses the glucose for energy. The increased insulin secretion from the pancreas and the subsequent cellular utilization of glucose results in lowered of blood glucose levels. Lower glucose levels then result in decreased insulin secretion 17
  18. 18. Continue……. If insulin production and secretion are altered by disease blood glucose dynamics will also change. Following meals, the amount of glucose available from carbohydrate breakdown often exceeds the cellular need for glucose. Excess glucose is stored in the liver in the form of glycogen, which serves as a ready reservoir for future use. When energy is required, glycogen stores in the liver are converted into glucose via glycogenolysis 18
  19. 19. Continue……. The liver also produces glucose from fat (fatty acids) and proteins (amino acids) through the process of gluconeogenesis. Glycogenolysis and gluconeogenesis both serve to increase blood glucose levels. Thus, glycemia is controlled by a complex interaction between the gastrointestinal tract, the pancreas, and the liver Insulin is the only hormone that lowers blood glucose levels. The counterregulatory hormones such as glucagon, catecholamine's, growth hormone, thyroid hormone, and glucocorticoids all act to increase blood glucose levels 19
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  22. 22. CLINICAL MANIFESTATION The symptoms are similar in type 1 & Type 2, but may vary in their intensity. (Common symptoms include polyuria and polydipsia, which are a consequence of osmotic diuresis. Blurred vision may occur due to a change in refraction. Weight loss despite normal or increased appetite is also common feature). Type 1 Type 2 22
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  24. 24. Patient's Blood glucose conditio levels n Inferences Fasting Fasting <110 mg/dl Normal value 110-126 mg/dl Impaired fasting glucose (IFG) value. Likely to develop NIDDM in later stages. Fasting 2hrs after glucose administration 126 mg/dl DM is indicated & must be confirmed (a) <140 mg/dl (b) 140-200 mg/dl (c) 200 mg/dl Normal glucose tolerance Impaired glucose tolerance (IGT) Diabetes mellitus is confirmed 24
  25. 25. HbA1c- THE BLOOD TEST What is HbA1c? Hemoglobin is a protein that makes your red blood cells red-colored. When hemoglobin picks up glucose from your bloodstream, the hemoglobin becomes glycosylated. HbA1c in your bloodstream Glycosylated hemoglobin is HbA1c. The HbA1c test measures the percentage of HbA1c in your blood— a number that corresponds to your average blood 25 glucose for the previous 3 months.
  26. 26. MANAGEMENT OF DM 26
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  28. 28. DIET Fresh vegetables with out salt & sugar sweets and chronic alcohol intake Green leafy vegetables Whole fruits than juices Citrus fruits Whole grain foods Beans-good source of fiber Chicken with skin Fish and lean cut beef & pork 28
  29. 29. Sulphonyl urea's Biguanides Meglitinides Tolbutamide Phenformin Repaglinide α-glucosidase inhibitors Chlorpropamide Metformin Nateglinide Acarbose Miglitol Acetohexamide Glibenclamide Glipizide Thiazolidinediones(TZD)/glitazones Ciglitazone Pioglitazone Troglitazone Rosiglitazone 29
  30. 30. INSULIN THERAPY Pancreas is an exocrine gland secreting pancreatic fluid Into the duodenum after a meal. Inside the pancreas are millions of clusters of cells called islets of Langerhans. The islets are endocrine tissue containing four types of cells. In order of abundance, they are: Who need insulin •Beta cells- insulin and amylin; medicine???? Type I (insulin dependent) diabetes •Alpha cells- glucagon; patients whose body produces no •Delta cells- somatostatin insulin. •Gamma cells/F cells- a polypeptide. Type 2 diabetes patients that do not always produce enough insulin. Treatment : subcutaneous injection 30
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  32. 32. •It stimulates skeletal muscle fibers. •It stimulates liver cells. •It acts on fat cells •It inhibits production of certain Regular insulin's Humulin enzyme. Novalin •In each case, insulin triggers these Neutral protamine hagedron Lente insulin(Zn) effects by binding to the insulin receptor. Insulin Analogs: Fatty acid acylated insulins Insulin lispro Insulin aspart Insulin glargine Insulin detemir 32
  33. 33. Diabetes Management Algorithm 33
  34. 34. Hypoglycemic coma Diabetic ketoacidosis Diabetic retinopathy  Diabetic nephropathy  Diabetic neuropathy  Diabetic foot ulceration  Diabetic Dermopathy  Diabetic CV diseases 34
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  37. 37. DIABETIC NEPHROPATHY is initially manifested by proteinuria & microalbuminuria. •Subsequently, as kidney function declines, urea and creatinine accumulate in the blood. PROGRESSIVE DIABETIC NEPHROPATHY consists of proteinuria of varying severity occasionally leading to nephrotic syndrome with hypoalbuminemia, edema, and an increase in circulating LDL cholesterol 37
  38. 38. •Loss of function appears which is due to an axonal neuropathic process. •Longer nerves are especially vulnerable, hence the impact on the foot. •Both motor and sensory nerve conduction is delayed and ankle jerks may be absent. •Sensory involvement usually seen which is associated with dulled perception of vibration, pain, and temperature. PAINFUL DIABETIC NEUROPATHY Erectile dysfunctioning is Hypersensitivity to light touch and occasionally severe "burning" pain, particularly at night, can become physically and emotionally disabling. Amitriptyline, 25-75 mg at bedtime, has been recommended for pain associated with diabetic 38 neuropathy
  39. 39. A foot ulcer in a diabetic patient, most probably due to nerve damage. The callus (hard skin) around the ulcer, indicating that the foot was subjected to excess pressure. 39
  40. 40. Skin spots are uncommon in adult diabetics. They are brownish, rounded, painless atrophic lesions of the skin in the pretibial area. Candidal infection can produce erythema and edema of intertriginous areas below the breasts, in the axillas, and between the fingers. It causes vulvovaginitis in most chronically uncontrolled diabetic women with persistent glucosuria and is a frequent cause of pruritus. While antifungal creams containing miconazole or clotrimazole offer immediate relief . Vulvovaginitis, recurrence is 40
  41. 41. •Cardiovascular disease risk is increased in patients with type 1 diabetes & risk is lower than in patients with type 2 diabetes. • Premenopausal women who normally have lower rates of coronary artery disease lose this protection once diabetes develops. •The increased risk in patients with type 2 diabetes reflects the combination of hyperglycemia, hyperlipidemia, abnormalities of platelet adhesiveness, coagulation factors, hypertension, oxidative stress, and inflammation. •Lowering LDL cholesterol reduces without known 41 coronary disease
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  55. 55. REFERENCES •The Pharmacological basis of Therapeuties    -    Goodman and Gilman's •The Pharmacological basis of Therapeuties    -    Goodman and Gilman's •Robbins Basic pathology •Robbins Basic pathology •Pharmaco therapy –– A pathophysiological approach –– Joseph. T. Dipiro •Pharmaco therapy A pathophysiological approach Joseph. T. Dipiro •Clinical Pharmacy and Therapeuties by Roger Walker •Clinical Pharmacy and Therapeuties by Roger Walker •Chehade JM, Mooradvan A.D, aa rational approach to drug therapy of type 22 •Chehade JM, Mooradvan A.D, rational approach to drug therapy of type diabetes mellitus. Diabetes metab 2000; 105-131 diabetes mellitus. Diabetes metab 2000; 105-131 •Doyle ME, Egan J.M, pharmacological agents that directly modulate insulin •Doyle ME, Egan J.M, pharmacological agents that directly modulate insulin secreation. Pharm Rev.2003, 50:105-131 secreation. Pharm Rev.2003, 50:105-131 •Cusi K, Defronzo RA, metformin: A review of its Metabolic effects Diabetes •Cusi K, Defronzo RA, metformin: A review of its Metabolic effects Diabetes reviews 1998; 6:89-131. reviews 1998; 6:89-131. •National Diabetes Fact sheet: Genaral information and National estimates on •National Diabetes Fact sheet: Genaral information and National estimates on diabetes in the United States, 2003 Atlanta, GA:US. Department of Health diabetes in the United States, 2003 Atlanta, GA:US. Department of Health and Human Service. and Human Service. •Rorine M, Letiexhe MR, Scheen AJ, Ziegler O. Obesity and type 22 diabetes •Rorine M, Letiexhe MR, Scheen AJ, Ziegler O. Obesity and type diabetes RW. Med Liege.2005;60:374-382. RW. Med Liege.2005;60:374-382. •INT.J.DIAB.DEV.COUNTRIES(2003), VOL. 23 •INT.J.DIAB.DEV.COUNTRIES(2003), VOL. 23 •American Diabetes Association. Diagnosis and classification of diabetes55 •American Diabetes Association. Diagnosis and classification of diabetes mellitus. Diabetes care 2004; 27(suppl.1):S5 – S10.
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