Diabetes : PCC Module B

1. Counseling by Retail Pharmacist to Diabetic Patients Diabetes : PCC Module B

2. One whole day session 10 am to 4 pm with lunch break: THURSDAY Topics: Cardiovascular Disorders (Hypertension, Hyperlipidemia, MI, Angina) Points to cover: Pathophysiology of disease (45 min each + 10 min queries) Therapeutics (Medicines used in treatment) 40 min+10 min queries Case studies with real prescriptions Counseling to real patients Experience sharing by participants on patients till date Faculty: Raj Vaidya, Dr.Adepu Ramesh Diabetes : PCC Module B

3. Two Half-day sessions on same day (total one full day): FRIDAY Topics: ONE: Diabetes (Pathophysiology, Therapeutics, Case studies and Counseling to real patients) Faculty: Dr.Ramesh, Raj Vaidya and physician if required LUNCH BREAK TWO: Asthma ((Pathophysiology, Therapeutics, Case studies and Counseling to real patients) Faculty: Dr.Ramesh, Raj Vaidya, and physician if required Diabetes : PCC Module B

4. One whole day session 10 am to 4 pm with lunch break: SATURDAY ONE: Tuberculosis: (Pathophysiology, Therapeutics, DOTS card and Counseling to pseudo patients) Faculty: Dr.Ramesh, Mrs.Manjiri and Chest physician if required LUNCH BREAK TWO: HIV/AIDS ((Pathophysiology, Therapeutics, Counseling to pseudo patients) Faculty: Raj Vaidya, Dr.Sampada and AVERT physician if required Last session (additional if permitted) on ADR Reporting by Retail Pharmacists (Dr.Ramesh) Diabetes : PCC ModuleB

5. Management of the Diabetic Patient

6. WHAT YOU NEED TO KNOW ABOUT DIABETES • WHAT IS DIABETES? • Commonly known as having Sugar Diabetes or Madhumeh in Hindi. • It is a disease in which the body either does not produce enough insulin or is unable to use the insulin the way it should be. • Insulin is a hormone produced in the pancreas, that helps the body to convert the glucose into energy. Diabetes : PCC Module B

7. Diabetes • Diabetes has two components: Metabolic and Vascular. • The metabolic component consists of elevation of blood glucose associated with alterations in lipid protein metabolism, resulting from a relative or absolute lack of insulin. • The vascular component includes the microvascular disease of the kidney and the eye as well as with premature macrovascular pathology and serious microangiopathy pathology. Diabetes : PCC Module B

8. Diabetes Etiology • Diabetes may result from any of the following: • Autoimmune disorder • Primary destruction of islet cells by inflammation, cancer, or surgery • Endocrine condition such as hyperpituitarism or hyperthyroidism • Iatrogenic disease following the administration of steroids

9. Pathophysiology of Diabetes • Glucose is the major fuel for the body and the most important stimulus for insulin secretion. • When levels exceed 180mg/100ml, glucose is excreted into the urine which results in increased urinary volume • This increase leads to dehydration, and loss of electrolytes

10. Pathophysiology of Diabetes • Insulin is needed for muscle, fat, and liver to utilize glucose from the blood. The CNS and renal cortex, however, can utilize glucose from blood without insulin. • Insulin is released from islet cells of Langerhan in the pancreas to have 4 actions: • Transfer glucose from blood to insulin-dependent tissues • Stimulate transfer of amino acids from blood to cells • Stimulate triglyceride synthesis from fatty acids • Inhibit breakdown of triglycerides for mobilization of fatty acids

11. Pathophysiology of Diabetes Without insulin, cells are impermeable to glucose and they begin to breakdown triglycerides into fatty acids, the byproducts of this gives rise to Ketoacidosis.

12. Type I Diabetes • Insulin is virtually absent • Plasma glucagon is elevated • Pancreatic Beta cells fail to respond to all insulingoenic stimuli

13. Type I Diabetes • Onset usually before 40, most likely children and teenagers • Polyuria, polydipsia, increased fat metabolism, • Prone to ketoacidosis • Caused by: Genetic predispositionHLA, Extrinsic factors: viral (mumps, Coxsackie's, CMV, hepatitis) • Require exogenous insulin replacement

14. Type II Diabetes • Tissue insensitivity to insulin • Deficiency in the response of pancreatic B cells to glucose • Etiology: Obesity, Genetics • Accounts for more than 90% of all Diabetics

15. Type II Diabetes • Onset is usually adulthood • Tendency to be obese • Polyuria, polydipsia, but usually not prone to ketoacidosis • Treatment is usually weight loss, diet restrictions, and oral hypoglycemics

16. Genetic Defects of pancreatic B cell function Diseases of the exocrine pancreas Endocrinopathies i.e.) Acromegaly, Cushing's Genetic Defect in insulin action Drug or chemical induced Other genetic syndromes i.e.) Downs, Turner’s Other Specific Types

17. Polyuria and polydipsia(thirst) -due to osmotic diuresis secondary to sustained hyperglycemia Results in loss of glucose, water, and electrolytes Polyphagia (eating too much)- initially due to depletion of water, glycogen, and triglycerides Then due to reduced muscle mass as amino acids are diverted to form glucose, and ketone bodies Signs and Symptoms

18. Weakness and Postural Hypotension-due to lowered plasma volumes, total body potassium loss, and general catabolism of muscle protein Recurrent blurred vision- lenses and retinas are exposed to hypermolar state Paresthesias Signs and Symptoms

19. Signs and Symptoms • Macrovascular Disease (atherosclerosis)-found in individuals with uncontrolled diabetes • Increased levels of LDL • Increased risk of ulceration and gangrene of the feet, HTN, renal failure, coronary insufficiency, MI, and CVA • MI is the leading cause of death in Type II patients HTN-Hypertensive Crisis: The brain is particularly vulnerable to the effects of severe hypertension. Extremely high BP—greater than 180/110 mm Hg—damages blood vessels; the vessels become inflamed and may leak fluid or blood into the brain, leading to stroke and, along with it, lasting disability. CVA-Cerebrovascular accident: The sudden death of some brain cells due to lack of oxygen when the blood flow to the brain is impaired by blockage or rupture of an artery to the brain. A CVA is also referred to as a stroke.

20. Signs and Symptoms • Microvascular disease • Thickening of intima • Endothelial proliferation • Lipid depositions • Mostly effects the retinas and small vessels of the kidneys

21. Signs and Symptoms Diabetic Retinopathy • Reflects the rate of absorption, uptake by tissue and excretion in urine • Nonproliferative changes i.e.) microaneruysms, retinal changes • Proliferative changes i.e.) neovascularization

22. Signs and Symptoms Diabetic Nephropathy • Sustained hyperglycemia leads to increased albumin levels. This decreases GFR and leads to ESRD. • Leading cause of death in Type I Diabetes

23. End-stage renal disease is when the kidneys permanently fail to work. • Symptoms of ESRD: • poor appetite • vomiting • bone pain • headache • insomnia • itching • dry skin • malaise • fatigue with light activity • muscle cramps • high urine output or no urine output • recurrent urinary tract infections • urinary incontinence • pale skin • bad breath • hearing deficit • detectable abdominal mass • tissue swelling • irritability • poor muscle tone • change in mental alertness • metallic taste in mouth

24. Signs and Symptoms Diabetic Neuropathy • Muscle Weakness, Muscle cramps, deep burning pain, tingling sensation, numbness • Loss of intestinal mobility, gastric distention, sexual impotence, bladder dysfunction, esophageal dysfunction

25. Diabetic Ketoacidosis • Leads to decrease in the blood’s pH or metabolic acidosis. As the blood levels of ketoacids rises, the blood pH drops below 7.3, and induces hyperventilation • Signs: anorexia, nasuea/vomitting, polyuria, tachypnea, dehydration, and coma • Patients may have sweet or fruity breath due to the byproduct acetone

26. Oral Signs and Symptoms • Poor Wound Healing • Periodontal Disease-usually in poorly controlled or undiagnosed diabetics • Incidence of Perio Disease increases among patients with diabetes as they age • Diabetics with advanced systemic conditions have periodontal disease more frequently and severe.

27. Diagnosing the Diabetic • Symptoms of Diabetes and non-fasting plasma glucose concentration is 200mg/ml or greater • Fasting glucose is 126mg/dl • Lowered oral glucose tolerance test (after 75g glucose load) blood glucose is 200mg/dl or greater

28. Diagnosing the Diabetic • Glycosylated Hemoglobin Hb1Ac • Glycohemoglobin increases in presence of hyperglycemia • Levels help monitor progress of disease and level of patient control • Reflects glucose levels in blood over 6-8 weeks preceding the test

29. Treatment Modifications • Short morning appointments • Instruct patient to eat normal AM meal • Frequent hygiene recalls • Stress reduction protocol • Antibiotic management for acute infections

30. If fasting glucose levels are less than 70 mg/dl, defer elective treatment and give patient carbohydrates If fasting glucose is above 200 mg/dl, defer elective treatment and give patient hypoglycemic agent Refer to physician Elective treatment

31. Hypoglycemia presents with: Nervousness Sweating Tremor Headache Confusion decreased respiration Treatment of the conscious patient includes giving oral carbs, and continue assessing vitals Unresponsive patient-activate ABC’s, and administer parenteral carbohydrates Managing the Hypoglycemic Emergency

32. Blood glucose levels greater than 250 mg/dl Dry, warm skin Hyperventilation Fruity, sweet breath Rapid weak pulse, and normal to low BP Conscious patient-supportive care Unconscious patient- ABC’s, Call hospital Do not administer insulin Start IV of 5% Dextrose and normal saline before EMT arrive Managing the Hyperglycemic Diabetic

33. THERAPEUTICS Diabetes : PCC Module B

34. TREATMENT OPTIONS • LIFE STYLE CHANGES • 􀂄 • Weight Reduction • 􀂄 Diet • 􀂄 Diet + Exercise • 􀂄 Diet + Exercise + Medicines Diabetes : PCC Module B

35. MANAGEMENT OF LIFE STYLE CHANGES • Counseling With A Registered Dietician • Stress management and yoga Food Guide Pyramid: Asian

36. What You Should Eat Every Day on a Vegetarian Diet. Food Pyramid: Vegetarian • A small amount of vegetable oil and margarine /butter. • 2 servings of milk, cheese, eggs or soy products • 2 or 3 servings of pulses, nuts & seeds • 4 or 5 servings of fruit and vegetables • 3 or 4 servings of cereals/grainsor potatoes • Some yeast extract fortified with vitamin B12.

37. MEDICATIONS USED TO TREAT TYPE 2 DIABETES • Sulfonylureas: • Tolbutamide or Orinase • Tolazamide or Tolinase • Chlorprpamide or Diabenese • Second generation Sulfonylyreas: • Glipizide or Glucotrol, Glucotrol XL • Glyburide or Diabeta, Micronas • Glimepiride or Amaryl • Biguanides • Metformin or Glucophage • Metformin ER or Glucophage XR

38. MEDICATIONS USED TO TREAT TYPE 2 DIABETES • Thiazolidinediones: • Rosiglitazone or Avandia • Pioglitazone or Actos • Alpha glucosidase inhibitors: • Acarbose or Precose • Miglitol or Glyset • Combination oral anti diabetic meds on the market • Glucovance ( Glyburide + Metformin) • Avandamit (Rosiglitazone + Metformin) • Insulin Injections • Short acting like Humolog and Novolog • Long acting like NPH and Lente • Glarzine (Lantus) once daily

39. BMI or Body Mass Index • Calculated by weight in kilos divided by height in meters squared • Normal BMI =18.5 to 24.9 • Over weight= 25 to 29.9 • Class I obesity= 30 to 34.9 • Class II obesity= 35 to 39.9 • Class III obesity or Morbid obesity is BMI of 40 and over Diabetes : PCC Module B

40. METABOLIC SYNDROME • Hypertension • Dyslipidemia (low HDL, High TG) • Waist measurement more than 35” for women and more than 40” for men • For Asian women, waist more than 32.5” and higher than 35” for men • Insulin resistance

41. PRE DIABETES • Fasting Blood sugar 120 to 125 on 2 separate occasions • 2 hour OGTT 140 to 199 • Usually asymptomatic • SIGNIFICANCE OF DETECTING PRE DIABETES • Converts to diabetes in 4 to 7 years • Can be delayed with life style changes and weight loss of 5 to 10% of body weight. • Medication use may be indicated • Early treatment can delay complications from diabetes

42. REGULAR MONITORING • Weight • BP • Foot examinations • Pulse rate • Sores, calluses • Test for sensations • Annual eye exams by ophthalmologist • Hemoglobin A1 C every 3 to 6 months • Annual fasting lipid panels • Urine test for presence of proteins 􀂄

43. GOALS FOR TREATMENT • Control of Blood Sugar (HgA1C below7) • Prevent end organ damage • Decrease morbidity