diabetes mellitus
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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: ManagementBasics:
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 IISulfonylureas: 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
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