Transcript DIABETES MELLITUS

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 510 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
Fast acting:
Lispro
Aspart
Long acting
Glargine
Ultralente
Short acting
regular
Intermediate acting
NPH
Lente
hours to onset
time to peak
time effective
<0.25 (15min)
0.17-0.33
0.5-1.5
0.67-0.83
3-4 (max 4-6)
1-3 (max 3-5)
2
6-10
none
10-16
24
18-20 (max 20-24)
0.5-1.0
2-3
3-6 (max 6-8)
2-4
3-4
6-10
6-12
10-16 (max 14-18)
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
from fluid retention)
(not thiazolidinediones because of risk of CHF
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
Microvascular
diabetic 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 20g/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