dr. escher

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.


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.


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.


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


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


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)


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)


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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