DIABETES MELLITUS ISSUES IN THE LONG TERM CARE SETTING AND ALLIED VENUES
DIABETES MELLITUS Focus: diabetes in the Medicare population
DIABETES MELLITUS Definition: a metabolic disorder in which there is deficiency of insulin production or resistance of organs to the effect of insulin
DIABETES MELLITUS • Diabetes is a disorder of metabolism--the way our bodies use digested food for growth and energy. • Most of the food we eat is broken down into glucose, the form of sugar in the blood. • Glucose is the main source of fuel for the body. • <http://diabetes.niddk.nih.gov/dm/pubs/overview/index.htm#what>
DIABETES MELLITUS • After digestion, glucose passes into the bloodstream, where it is used by cells for growth and energy. • For glucose to get into cells, insulin must be present. • Insulin is a hormone produced by the pancreas, a large gland behind the stomach. • <http://diabetes.niddk.nih.gov/dm/pubs/overview/index.htm#what>
DIABETES MELLITUS • NORMAL: When non-diabetic people eat, the pancreas automatically produces the right amount of insulin to move glucose from blood into our cells. • <http://diabetes.niddk.nih.gov/dm/pubs/overview/index.htm#what>
DIABETES MELLITUS • DIABETES: In people with diabetes, when they eat, the pancreas either produces little or no insulin, or the cells do not respond appropriately to the insulin that is produced (or both) => glucose builds up in the blood, overflows into the urine, and passes out of the body in urine => body loses its main source of fuel even though blood contains large amounts of glucose. • <http://diabetes.niddk.nih.gov/dm/pubs/overview/index.htm#what>
DIABETES MELLITUS (DM) • TYPES OF DIABETES • Type I • Type II • MODY (Maturity Onset Diabetes of Youth • Gestational
DM TYPE I Auto-immune disease Constitutes 5-10% of DM diagnosed in the USA Mostly appears in children and young adults Develops as a result of auto-immune destruction of beta-cells in the pancreas Presents with polyuria, thirst, weight loss, marked fatigue Can be complicated by coma with ketoacidosis • <http://diabetes.niddk.nih.gov/dm/pubs/overview/index.htm#what>
DM TYPE II • Most common form of diabetes • Involves about 90-95% of people with DM • Associated with: • older age • obesity • family history of DM • prior history of gestational diabetes • physical inactivity • ethnicity • <http://diabetes.niddk.nih.gov/dm/pubs/overview/index.htm#what>
DM TYPE II • Patient with type II DM usually makes enough insulin but the body cannot use it effectively => insulin resistance • Gradually insulin production decreases over the following years • Symptoms are similar to type I but develop more gradually • <http://diabetes.niddk.nih.gov/dm/pubs/overview/index.htm#what>
DM TYPE II • Symptoms of type II DM include: • Fatigue • Nausea • Frequent urination/polyuria • Thirst • Unusual weight loss • Blurred vision • Frequent infections • Slow healing of wounds or sores • Sometimes no specific symptoms • <http://diabetes.niddk.nih.gov/dm/pubs/overview/index.htm#what>
GESTATIONAL DIABETES • Develops only during pregnancy • More common in: • African Americans • American Indians • Hispanic Americans • women with a family history of diabetes • Women with a history of gestational diabetes have a 20-50% chance of getting type II DM within 5-10 years <http://diabetes.niddk.nih.gov/dm/pubs/overview/index.htm#what>
Diabetes Mellitus: Diagnosis • Fasting plasma glucose = preferred test: Positive test is glycemia of 126mg/dL or higher after fasting at least 8 hours • Random plasma glucose of 200mg/dL or higher along with symptoms of diabetes • Oral glucose tolerance test (OGTT) plasma glucose of 200mg/dL or higher done 2 hours after ingestion of 75 grams of glucose in water • <http://diabetes.niddk.nih.gov/dm/pubs/overview/index.htm#what> • MKSAP13 Endocrinology and Metabolism. American College of Physicians 2004.
Diabetes Mellitus • Hemoglobin A1c measurement is not recommended currently for diagnosis of diabetes. • HbA1c is used as a marker to monitor glycemia control in patients over time • MKSAP13 Endocrinology and Metabolism. American College of Physicians 2004.
Pre-Diabetes • Pre-diabetes refers to a state between “normal” and “diabetes” = fasting plasma glucose 100-125mg/dL (higher than normal but not high enough for diagnosis of diabetes) Affects about 41 million people in USA(previously referred to as either impaired fasting glucose or impaired glucose tolerance) • http://diabetes.niddk.nih.gov/dm/pubs/overview/index.htm#types • MKSAP13 Endocrinology and Metabolism. American College of Physicians 2004.
Type II Diabetes Diagnostic testing - when to do it: People 45 years old => if normal then every 3 years MKSAP13 Endocrinology and Metabolism. American College of Physicians 2004.
Type II Diabetes: diagnostic testing Younger than 45 yo or more often than every 3 years if: overweight first degree relative with diabetes member of high risk ethnic group (Afro-American, Hispanic American, Native American, Asian American, Pacific Islander) delivered a baby 9 lbs. gestational diabetes hypertensive (BP 140/90mmHg) High Density Lipoprotein cholesterol 35mg/dl or less TriGlyceride level 250mg/dl or more pre-diabetes MKSAP13 Endocrinology and Metabolism. American College of Physicians 2004.
DM type II: Management Basics: healthy eating physical activity blood glucose testing Pharmaceuticals: oral medication(s) insulin(s) both oral medicines and insulin
DM: insulin variations Daily insulin requirements are influenced by: diet exercise stress
Diabetes Management: Stress Stress influences response to insulin Stress => increased cortisol increased catecholamines increased growth hormone => these hormones all lead to increased insulin resistance (thus, hyperglycemia)
Control of Diabetes Control of Diabetes includes: glycemia control (FBS < 126mg/dL; HbA1c <7%) weight management blood pressure control (BP < 130/80mmHg) lipid management reduction in the hypercoagulable state (aspirin or clopidogrel)
DM type II: Management Most people with newly discovered type II DM are overweight Basics are diet and exercise: nutrition life style modification increased physical activity Goal = Hemoglobin A1c < 7% If this goal in not reached and maintained => pharmacotherapy (medications)
Insulins Type hours to onset time to peak time effective Fast acting: Lispro <0.25 (15min) 0.5-1.5 3-4 (max 4-6) Aspart 0.17-0.33 0.67-0.83 1-3 (max 3-5) Long acting Glargine 2 none 24 Ultralente 6-10 10-16 18-20 (max 20-24) Short acting regular 0.5-1.0 2-3 3-6 (max 6-8) Intermediate acting NPH 2-4 6-10 10-16 (max 14-18) Lente 3-4 6-12 12-18 (max 16-20) MKSAP13 Endocrinology and Metabolism. American College of Physicians 2004.
Insulin Insulin dependency regimens - examples: 1. insulin glargine q24h and pre-meal insulin 2. NPH and regular before breakfast and supper 3. Rapid or short acting insulin before meals & intermediate acting insulin (NPH or Lente) at bedtime 4. Insulin Glargine at bedtime and rapid or short acting insulin before meals Insulin regimens depend on individual patient requirements
Medications for DM type II Sulfonylureas & Meglitinides: promote glucose-stimulated release of insulin from pancreas (they need enough remaining beta-cell function in the pancreas to work) (insulin secretogogues) Metformin: mostly blocks gluconeogenesis in the liver; also interferes with glycogenolysis and improves insulin sensitivity of muscle Thiazolidinediones: bind to nuclear receptors in tissues & activate or suppress expression of specific genes (insulin sensitizers) - risk of fluid retention & weight gain; 4-12 week latency to work; monitor liver enzymes q2mo Acarbose: alpha-glucosidase inhibitor; interferes with intestinal absorption of carbohydrates; causes flatulence & bloating (discontinuation) MKSAP13 Endocrinology and Metabolism. American College of Physicians 2004.
Medications for DM type II Sulfonylureas: insulin secretogogues glyburide glipizide glimeperide chlorpropamide Meglitinides: insulin secretogogues repaglinide nateglinide Biguanide: decreases hepatic gluconeogenesis metformin Thiazolidinediones: insulin sensitizers pioglitazone rosiglitazone Alpha-glucosidase inhibitor: decreases GI absorption of carbohydrate acarbose;
Insulin in Type II DM Usually indicated if HbA1c > 7% despite life style modification and 2 oral medications May be postponed in borderline cases where HbA1c is < 8.5% pending addition of a 3rd oral agent; otherwise => Addition of bedtime dose of basal insulin therapy (glargine) to sulfonylureas +/- metformin(not thiazolidinediones because of risk of CHF from fluid retention)
The Metabolic Syndrome • Hypertension • Visceral (central) obesity • Hypertriglyceridemia • Low HDL cholesterol • Insulin resistance or glucose intolerance • Prothrombotic state (high fibrinogen or plasminogen activator inhibitor [-1] in blood) • Proinflammatory state (high C-reactive protein in blood) • http://www.americanheart.org/presenter.jhtml?identifier=4756
Acute Complications of type II DM Hyperglycemic hyperosmolar state: common in elderly triggered by underlying disorder(s) risk increased in elderly due to decreased thirst reflex often complicated by delirium
Acute Complications of type II DM Hyperglycemic hyperosmolar state: serum osmolarity > 320 mosm/L plasma glucose > 600mg/dL dehydration no ketoacidosis underlying disorder(s)
Hyperosmolar State Therapy: rehydration with hypotonic solution insulin infusion (initially) watch for signs of fluid overload/CHF monitor potassium treat underlying cause (eg UTI, cellulitis)
Hypoglycemia Hypoglycemia = plasma glycemia < 50mg/dL with or without symptoms More common in type I DM and patients with significant renal or liver disease Another reason for glucose monitoring Treated with po sugar (e.g. fruit juice or glucose tablets) or IV dextrose 50% in water or IV glucagon or both
Complications of DM Chronic complications of diabetes mellitus include: Macrovascular Microvascular Neuropathic
Complications of DM Macrovascular atherosclerosis/cardiovascular disease peripheral vascular disease
Complications of DM Microvasculardiabetic retinopathy: due to ischemia of retna; provokes neovascularization with vessels more fragile => leaking => scarring & fibrosis diabetic nephropathy: common cause of ESRD; prevention via control of blood pressure and glycemia; earliest signs urine albumin 30mg/day or 20g/min; appears to benefit from ACE-I’s and ARB’s too
Complications of DM Diabetic Neuropathy peripheral sensory neuropathy cardiovascular autonomic neuropathy gastrointestinal autonomic neuropathy erectile dysfunction mononeuropathy diabetic foot
Complications of DM Peripheral sensory neuropathy variable presentation dysesthesia tingling pain loss of pain sensation (risk of injury)
Complications of DM Cardiovascular Autonomic Neuropathy orthostatic hypotension lack of normal variation in heart rate with breathing, tachycardia
Complications of DM Gastrointestinal Autonomic Neuropathy gastroparesis: nausea, bloating, vomiting (tx metoclopramide) diarrhea: often nocturnal
Complications of DM Erectile dysfunction: autonomic neuropathy absent nocturnal and morning erections more common than diagnosed
Complications of DM Mononeuropathy acute local pain distribution of a nerve may recede if treated early with improved glucose control (glucotoxicity)
Complications of DM Diabetic Foot sensory deficit (skin, bone, ligament) fungal infection wounds pulses (PVD) slow healing ulcers
Type II DM: Goals Prevention of pre-diabetes Prevention of change from pre-diabetes to diabetes Diagnosis through screening Early management/therapy Prevention of complications
Type II DM: Goals Screening via fasting glycemia and history Life-style history and modification Physical activity Diet Treatment of glycemia, lipids, hypercoagulable state, blood pressure Management of complications