Geriatric Endocrinology

Himawan Sanusi

Endocrinology and Metabolism

Internal Medicine
Medicine Faculty
Hasanuddin University
Geriatric endocrinology

• Diabetes mellitus
• Thyroid
Type 2 DM : a silent killer

 30 % of people T2DM are not diagnosed

 50 % of those diagnosed with T2DM already

have advanced disease with signs of
complications

 65-80 % of T2DM  cause of death CVD

 2-4 x of T2DM risk of CVD and 2X stroke

National Institute of Diabetes and Digestive and Kidney Diseases. http://diabetes.niddk.nih.gov/
dm/pubs/statistics/index.htm#7 [Accessed 1 December 2005]
Wingard DL et al. Diabetes Care 1993;16:1022-5
 Diabetes prevelance

Engelgau MM et al. The evolving diabetes burden in the US. Ann Intern Med.2004;140:945
Diabetes in elderly
Prevalence
 The prevalence of diabetes mellitus
increases with age
 The National Health and Nutrition
Examination Survey (NHANES) of 1999–
2000 suggested that 38.6% of people over
the age of 65 have diabetes
 The prevalence is higher in some minority
racial and ethnic groups, including African
Americans, Hispanics, and Native Americans
Prevalence of DM in
elderly
 USA : estimated at 7 million / 20% of
all people 65 y.o. and older
 Decline slightly in those older than 75
compared with those 65 – 74 y.o.
 Decreases further in those older than
85
Why elderly people

Type 2 DM
 Diabetes Mellitus in elderly

“Healthy” elderly individuals demonstrate :

• age-related increase in fasting blood
glucose  1 mg/dl per decade and
• a more significant increase in blood
glucose  5 mg/dl per decade in response
to a standard glucose tolerance test
 Pathogenesis
b-cell Of Type 2 DM Insulin
dysfunction resistance
Lipotoxicity
Gluconeo VLDL Increased
genesis lipolysis
+ Elevated
Elevated
Plasma
Glucose toxicity + TNF-a,leptin
FFA
-
decreased
Increased hepatc glucose uptake
glucose output Adipose tissue
Reduced plasma (Obesity)
insulin

• Reduced GLP-1 secretion

Hyperglycemia (Type 2 DM)
• Enhanced Glucagon
 b Cell dysfunction in elderly
 Aging  w/
declining b cell
function and
relative insulinopenia
independent of
insulin resistance as
well as insulin
resistance itself
Insulin Resistance in elderly

The National Diabetes Data Group:

10% of the elderly have some degree of
glucose intolerance
Etiology:
- changes in body composition  muscle
mass decreases and body fat increases
- drugs
- decrease of physical activity,
- decreased insulin action.
 Age-related decreased
insulin secretion
Coexisting Age-related
illness insulin
resistance
Factors
predisposing
Genetics Adiposity
elderly to
changes in
diabetes body
composition

Drugs Decreased
physical activity

Factors predisposing elderly people to the development

of diabetes mellitus. Halter JB1990
Symptoms and Signs

• Asymptomatic : usually
• 3 P (polyphagic, polyuria, polydipsic)
• Weight loss, blurred vision
• Diabetic complication : UTI, skin infect,
etc.
When to perform D/ test ??

 The ADA also recommends diabetes

screening in :
– adults age 45 and older every 3 years
– subjects at high risk (family history of
coronary heart disease, cigarette smoking,
hypertension, obesity, kidney disease, and
dyslipidemia )  more frequent
 HOW
TO
DIAGNOSE
TYPE 2 DM IN ELDERLY
CRITERIA FOR THE DIAGNOSIS OF
DIABETES MELLITUS

1. Symptoms of diabetes (3 P)
Casual plasma glucose concentration >200
mg/dl
or
2. Fasting plasma glucose > 126 mg/dl
FPG, no caloric intake for at least 8 hours
or
3. 2-h post-OGTT > 200 mg/dl
75 gram glucose dissolved in water
 DIAGNOSIS OF
DIABETES MELLITUS
Elderly subjects are more glucose
intolerance, the diagnosis in the
elderly should be FPG and OGTT
Clinical Features

 Diagnosis should not be based on the

presence of glycosuria  renal threshold
for glycosuria increases in the elderly
 Complications of diabetes mellitus are
related to the duration of disease
 Hypoglycemia in the elderly is associated
with important sequelae
Treatment
 Maintain the fasting blood glucose below
150 mg/dL and the postprandial blood
glucose below 220 mg/dL and A1C < 7
 Therapy should :
– decrease hyperglycemic symptoms
– prevent infections
– prevent progression to nonketotic hyperosmolar
coma
 Appropriate control of blood pressure and
lipid levels.
Treatment Goals for Diabetic patients

• Symptom free
• Prevent short term complications (HONC)
• Prevent long term complications
• Quality of life = Lifestyle focus

Elderly T2DM maintain :

• fasting blood glucose below 150 mg/dL
• postprandial blood glucose 140 – 220 mg/dL
• A1c < 7
Treatment
 Lifestyle
modification
 Hyperglycemic lowering agents

 Insulin
 Meglitinides
Thiazolidinediones
Increase insulin secretion
Increase glucose uptake
from pancreatic b-cells
in skeletal muscle and
decrease lipolysis in
adipose tissue
Insulin secretagogue

Sulfonylureas
Increase insulin
secretion from Biguanide (metformin)
pancreatic b-cells Decreases hepatic
production and
increases glucose uptake

a-Glucosidase inhibitors
Delay intestinal
DPP – 4 inhibitor carbohydrate absorption

DPP-4 = Dipeptidyl peptidase – 4 inhibitior

Adapted from Cheng and Fantus. CMAJ. 2005;172:213–226
 Treatment
 Diabetic diets & exercise program 
initial therapy

 Hyperglycemic lowering agent if :

hyperglycemia persists (FBG 150–300
mg/dL)
Treatment
1. Sulfonylureas
1st generation : Chlorpropamide should be
avoided because of its long half-life and its
to induce both hyponatremia and
hypoglycemia.
2nd generation : glipizide and glimepiride
are often used  less hypog eff than
glibenclamide
– SU  start lower dose because
hypoglycemic effect
Hyperglycemic lowering agents
b) Glinid : repaglinid and nateglinid
Short half life, Hepatic excretion

c) Biguanide : metformin
Cr serum > 1.5 mg/dl, CHF, PPOK

d) a-glucosidase inhibitor : acarbose

Non absorbable

e) Thiazolidinedione : pioglitazone/rosiglitazone
Water retention

f) DPP - 4 inhib : vildagliptin or sitagliptin

 Treatment

 If the fasting blood glucose remains above 150

mg/dL on diet, exercise, and oral agent
therapy, insulin should be started in
combination with oral agents or by itself

 Because elderly patients often lack symptoms

of hypoglycemia, the fasting, postprandial, and
bedtime blood glucose levels must be checked
initially even if symptoms are absent
Treatment
 Control other adverse factors such as
hypertension, dyslipidemia, and smoking,
which can contribute to vascular complications
associated with diabetes
 ADA recommends aspirin therapy (81–325
mg/d) for primary prevention in high-risk
patients and for secondary prevention in
patients with macrovascular disease
 Good glycemic control can decrease
complications and reduce mortality
TREATMENT OF HYPERGLYCEMIA
IN ELDERLY T2DM
Caution :
- Organ failure : kidney and liver
- Others degenerative disease : CAD,
hypertension, dyslipidemia
- Drug interactions
Complications of DM in elderly

 Acute Complications
Hypoglycemia
Diabetic ketoacidosis
Hyperosmolar nonketotic coma
 Chronic Complication
Macro - Microvascular

Greenspan’s Basic & Clinical Endocrinology 2007:722-5

 Nonketotic Hyperosmolar
Coma
 Occurs almost exclusively in the elderly, one-third
of such patients have no previous history of
diabetes
 Predisposing factors :
Inadequate insulin secretion & reduction in the
peripheral effectiveness of insulin
 Precipitating event
– infection (32–60% of cases)  pneumonia,
abscess
– medication ( thiazide, furosemid, phenytoin,
glucocorticoid) or other acut medical illness
Nonketotic Hyperosmolar
Coma
Symptoms :
 acute confusional state, lethargy, weakness,
and occasionally coma.
 Neurologic findings can be generalized or
focal and can mimic an acute
cerebrovascular event.
 Marked volume depletion
 orthostatic hypotension
 prerenal azotemia
Treatment of Nonketotic
Hyperosmolar Coma

 Rehydration  normal saline infusion

( deficit amount 9 L), after 1-3 L given
 changes normal saline  NaCl
0.45%. Half of the fluid and ion
deficits should be replaced in the first
24 hours and the remainder over the
next 48 hours.
Treatment

 Insulin
Intravenous insulin in small doses (10–15
units) should be given initially, followed by a
drip infusion of 1–5 units/h
 Potassium deficits should be corrected
 Treating of precipitating event
 More than one-third of patients can be
discharged without insulin treatment
 Insulin Resistance
Insulin Glucose

receptor X

PPARg +RXR
X Synthesis GLUT 4
mRNA

PPRE transcription
promoter Coding reg

Modified from Howard L. Foyt et al. Thiazolidinediones. Diabetes Mellitus: a Fundamental and Clinical Text, 2nd Ed.
 Pioglitazone reduced Insulin resistance
Insulin Glucose

Insulin
receptor

PPARg +RXR
Synthesis GLUT 4
mRNA
Pio

PPRE transcription
promoter Coding reg

Modified from Howard L. Foyt et al. Thiazolidinediones. Diabetes Mellitus: a Fundamental and Clinical Text, 2nd Ed.