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Diabetes Mellitus

Introduction
The most common endocrine disorder in Indonesia Diabetes mellitus is a chronic incurable disease that results from deficits in insulin action or secretion or usage. An inadequate amount of insulin causes changes in metabolism Cause unknown, may be related to : heredity viruses autoimmune/immune factors Diabetes is leading cause of blindness, heart attack, stroke, and gangrene

Diabetes Mellitus
Glucose accumulates in the blood and excreted in the urine The body is required to use protein and fat for energy which leads to metabolic acidosis Insulin may not be produced by the islets of langerhans or production may be diminished which results in a high blood glucose

Classifications of Diabetes
Insulin dependent diabetes mellitus (IDDM) also called type one (I) diabetes previously called juvenile - onset or brittle diabetes usually occurs between the age of 5 to 11 usually thin, ketosis prone dependent on insulin for life !!!

Non insulin dependent diabetes mellitus (NIDDM) also called type two (II) diabetes previously called stable or adult onset diabetes usually over the age of 30, now seen in children usually the person is obese, not prone to ketosis insulin level may be normal ,but unable to enter the cell insulin level may also be low or high

Signs and symptoms


sudden onset of glucose levels in blood

polyuria - excessive urination polydipsia- excessive thirst polyphagia- excessive hunger no weight gain polyneuropaty - numbness or tingling sensation pruritus - itching

Diagnostic Tests
Signs and symptoms and random blood glucose at 200 or greater Fasting blood glucose at 140 or greater on two ocassions Elevated glucose level once after drinking 75 gr glucose at the 2 hour point in GTT (Glucose Tolerance Test) Glycosylated hemoglobin (HbA1c) reflection of how well the glucose has been controlled for the last 3 months - hyperglycemia causes an increase in HbA1c values expressed in percentages, with nondiabetic or well controled 5.5 to 6.0%, moderate controled 6.1 t0 8%, diabetic with poor control greater than 8.1%

Self glucose monitoring


provides patient with with current blood glucose level help patient maintain good gylcemic control requires patient to prick themselves several times a day instruct patient in proper procedure for obtaining glucose instruct patient to follow manufacturers instructions hands must be washed before and after procedure

Options for monotherapy

Sulfonylureas Meglitinides Biguanides Thiazolidinediones Alpha-glucosidase inhibitors

Mode of action

Sulfonylureas Meglitinides Stimulate insulin secretion Biguanides Thiazolidinediones Alpha-glucosidase inhibitors

Mode of action

Sulfonylureas Meglitinides Stimulate insulin more rapidly but less sustained Biguanides Thiazolidinediones Alpha-glucosidase inhibitors

Mode of action

Sulfonylureas Meglitinides Gluconeogenesis Glycolysis Glucose utilization Thiazolidinediones Alpha-glucosidase inhibitors Biguanides

Mode of action

Sulfonylureas Meglitinides sensitivity of peripheral tissue to insulin lipolysis Biguanides Thiazolidinediones Alpha-glucosidase inhibitors

Mode of action

Sulfonylureas Meglitinides Delay absorption of glucose from GIT Biguanides Thiazolidinediones Alpha-glucosidase inhibitors

Biguanides Decrease Hepatic Glucose Production Thiazolidinedinones (TZDs) Liver Increase Glucose Increased Glucose Uptake
Skeletal Muscle Decreased Glucose Uptake Production

TZDs Decreased Lipolysis


Adipose Tissue Increased Lipolysis

Sulfonylureas and Nonsulfonylurea Secretagogues Increase Insulin Secretion Pancreatic Beta Cells Insulin Secretion Defective Insulin Secretion

Lipotoxicity

Increased Free Fatty Acids

Lipotoxicity

Insulin resistant a-Glucosidase Inhibitors Delay Intestinal Carbohydrate Absorption


Small Intestine Carbohydrate Absorption

Hyperglycemia

Target Population

Sulfonylureas Meglitinides Recent type 2 DM diagnosis Type 2 DM < 5 years duration Biguanides Thiazolidinediones Alpha-glucosidase inhibitors

Target Population

Sulfonylureas Meglitinides Recent type 2 DM diagnosis Elevated PPG Biguanides Thiazolidinediones Alpha-glucosidase inhibitors

Target Population

Sulfonylureas Meglitinides Overweight/obese Insulin resistant Thiazolidinediones Alpha-glucosidase inhibitors Biguanides

Target Population

Sulfonylureas Meglitinides Insulin resistant Overweight Obese Thiazolidinediones Alpha-glucosidase inhibitors Biguanides

Target Population

Sulfonylureas Meglitinides Insulin resistant Overweight Obese Thiazolidinediones Alpha-glucosidase inhibitors Biguanides

Target Population

Sulfonylureas Meglitinides Elevated PPG Contraindications to other agents Biguanides Thiazolidinediones Alpha-glucosidase inhibitors

Advantages

Sulfonylureas Meglitinides Rapid FPG reduction Low cost Thiazolidinediones Alpha-glucosidase inhibitors Biguanides

Advantages

Sulfonylureas Meglitinides
Risk of hypoglycemia Short-acting Meal-adjusted dosing

Biguanides Thiazolidinediones Alpha-glucosidase inhibitors

Advantages

Sulfonylureas Meglitinides
No weight gain Risk of hypoglycemia

Biguanides Thiazolidinediones Alpha-glucosidase inhibitors

Advantages

Sulfonylureas Meglitinides Biguanides Amount of insulin Risk hypoglycemia Thiazolidinediones Alpha-glucosidase inhibitors

Advantages

Sulfonylureas Meglitinides Biguanides Risk of hypoglycemia Non systemic action Thiazolidinediones Alpha-glucosidase inhibitors

Disadvantages

Sulfonylureas Meglitinides
Weight gain Risk of hypoglycemia

Biguanides Thiazolidinediones Alpha-glucosidase inhibitors

Disadvantages

Sulfonylureas Meglitinides High costs Frequent dosing Thiazolidinediones Alpha-glucosidase inhibitors Biguanides

Disadvantages

Sulfonylureas Meglitinides GI side effects High costs Rare lactic acidosis Thiazolidinediones Alpha-glucosidase inhibitors Biguanides

Disadvantages

Sulfonylureas Meglitinides High cost Weight gain Slow onset of action Issue of liver toxicity Biguanides Thiazolidinediones Alpha-glucosidase inhibitors

Disadvantages

Sulfonylureas Meglitinides Biguanides High cost GI side effects Thiazolidinediones Alpha-glucosidase inhibitors

Total daily dose (mg) & dosing interval

Sulfonylureas Meglitinides Biguanides Glyburide 1.25 to 20 QD or BID Gliquidone 30 QD or BID (Glurenorm) Glipzide 2.5 to 40 QD or BID (Glucotrol) Thiazolidinediones Glipizide, extended-release 2.5 to 20 QD (Glucotrol XL) Glimepiride 1 to 8 QD (Amaryl) Gliclazide (Diamicron MR)

Alpha-glucosidase inhibitors

Total daily dose (mg) & dosing interval

Sulfonylureas Meglitinides Biguanides Nateglinide 180 to 360 TID (Starlix) Repaglinide 1.5 to 16 TID or QID (Novonorm)

Thiazolidinediones Alpha-glucosidase inhibitors

Total daily dose (mg) & dosing interval

Sulfonylureas Meglitinides Biguanides

Metformin HCI 1,000 to 2,550 BID or TID Thiazolidinediones Metformin, extended-release 1,000 to 2,000 QD or BID
Alpha-glucosidase inhibitors

Total daily dose (mg) & dosing interval

Sulfonylureas Meglitinides Rosiglitazone maleate 4 to 8 QD or BID (Avandia, Avandamet) Biguanides Pioglitazone HCI 15 to 45 QD (Actoz) Thiazolidinediones Alpha-glucosidase inhibitors

Total daily dose (mg) & dosing interval

Sulfonylureas Meglitinides Biguanides Acarbose 150 to 300 TID (Glucobay) Miglitol 150 to 300 TID Thiazolidinediones Alpha-glucosidase inhibitors

Monotherapy Pearls
All drugs except AGIs and nateglinide equally reduce HbA1c Metformin usually best for obese- no weight gain Non-SU secretagogues may be useful for irregular meals Metformin and TZDs avoid hypoglycemia

Clinical Efficacy of Oral Hypoglycemic Agents

Class of hypoglycemic agents


Sulfonylureas Meglitinides Biguanides Thiazolidinediones Alpha-glucosidase inhibitors

Reduction in HbA1c HbA1c (%)


0.8 to 2.0 0.5 to 2.0 1.5 to 2.0 0.5 to 1.5 0.7 to 1.0

Reduction in FPG (mg (mg per dl)


60 to 70 65 to 75 50 to 70 25 to 50 35 to 40

Options for combination therapy


Sulfonylureas + Biguanide or Thiazolidinedione or Alpha-glucosidase inhibitor Biguanide + Alpha-glucosidase inhibitor

Biguanide + meglitinide Biguanides + Thiazolidinediones

Triple combination therapy Sulfonylurea + biguanide + Thiazolidinedione or Sulfonylurea + biguanide + alphaglucosidase inhibitor

If therapeutic goals are not met using the above combinations; switch to insulin +/- oral agent

Insulin
made from the pancreas of pig or cow, or synthetically made can be stored at room temperature for up to a month do not expose to direct sunlight and keep away from heat store unopened and insulin that will last longer than a month in refrigerator monitor expiration date review SQ injection sites rotate site to prevent lipodystrophy begin teaching patient insulin administration immediately make sure patient can see lines on syringe and read label

Insulin
Short acting insulin Humalog - onset in 15 minutes, peaks a in 3 hours and duration is 5 hours Regular insulin (Actrapid, Humulin R) - onset is 30 minutes, peaks in 3 hours and duration is 6 hours Semilente - onset 30-60 minutes, peaks 5-7 hours and duration is 12-16 hours Intermediate acting insulin NPH - onset is 1-3 hours, peaks 8-12 hours and duration is 24 hours lente - onset 1-3 hours,peaks 7-15 hours and duration is 24 hours Long acting insulin Ultralente-onset is 4 hours,peaks in 16-22 hours and the duration is 36 hours. Lantus is new insulin given once a day and has no peak action. Premixed insulin 70/30 (30% Regular, 70% NPH)

Injection Sites
Deltoid-lateral surface of upper arms Abdomen Vastus lateralsis Upper back Upper buttocks

NOTE: Sites should be rotated to prevent lipodystrophy

Insulin Reaction
Hypoglycemia is the most common acute complication of diabetes bG is usually less than 60 (too little circulating glucose) Causes: too much insulin or diabetes medication, too much exercise, delayed or omitted food intake, alcohol consumption. When in doubt treat !!! S/S : dizziness, trembling sensation, sweating, irritability, headaches, blurred or double vision, pallor, palpitations, hunger. will lead to confusion, LOC, seizures

Insulin Reaction
Treatment must immediately raise the glucose simple carbohydrates juice, glucose tablets followed by complex carbohydrates glucagon preparation may be given 20-30 ml of 50% glucose solution (D50W) treatment may have rebound effect

Diabetic Ketoacidosis (DKA)


DKA lack of insulin and accumulation of glucose, waste products from Protein and fat metabolism. S/S begins with the 3 Ps, N/V, headaches, dry skin, weakness, flushed face F/E imbalance, dehydration, starvation, acid/base imbalance, sweet fruity breath, hypotension, increased heart rate, metabolic acidosis, ketones, kussmauls respirations. bG may be over 1000 mg/dl if S/S are unusual treat as hypoglycemia - this may lead to comatose state - treatment includes IV regular insulin by push or drip. - rapid infusion of IVFs to reverse dehydration .

Hyperglycemic Hyperosmolor, Nonketotic Coma (HHNC)


This is usually seen in NIDDM, more common in elderly, may be first sign of NIDDM. S/S --hyperglycemia, extreme dehydration. Treat with small amount of insulin, and massive amounts of fluid replacement. Discover cause

Chronic Complications
Neuropathy - peripheral nerves Retinopathy - eyes Nephropathy - kidney Macrovascular changes caused by atherosclerosis. Increase infections caused high bG

NOTE: Normal ranges in glucose prevents the above complications.

Foot Care
Wash feet daily with warm water and mild soap and dry well. Avoid hot water. Make sure area between toes are dry, do not apply lotion to this area. Consult a podiatrist for tough toenails or corns that require cutting. Inspect feet daily. Wear properly fitting shoes. Never soak feet or place heat on feet. Do not go barefoot. Avoid any constricting foot wear, socks, or hose.