DIABETES MELLITUS

Endocrine System
Secrete hormones ---> blood stream

Hormone release activated by trigger substances

PANCREAS - An Endocrine Gland

Islets of Langerhans

Beta Cells
Secrete INSULIN

Alpha Cells
Secrete GLUCAGON

INSULIN
Lowers blood sugar by: Transporting glucose into cell
Receptor sites
Converting glucose (little sugar) to glycogen (big sugar) for storage in
muscle and liver tissue (glycogenesis)
Converting excess glucose into fat cells, forming lipids from fatty acids
(lipogenesis) and promoting storage in adipose tissue

INSULIN
INHIBITS activity that causes the blood sugar to rise- - -

Stops: Conversion of stored glycogen to glucose in the liver

(Glycogenolysis)

Stops: Formation of new glucose or glycogen from non-

carbohydrate sources (Gluconeogenesis)
 GLUCAGON
Known as Hyperglycemic agent

Promotes activities that raise blood sugar- - -

Converting of stored glycogen to glucose (Glycogenolysis)
Formation of glucose from protein and fat sources (Gluconeogenesis)

Hormones affecting CHO (carbohydrate)

metabolism
ACTH (Adrenocorticotropic hormone) and Glucocorticoids (even
glucocorticoid/steroid medications)
enhance gluconeogenesis =
Raise Blood Sugar (by making new little sugars from fats/proteins)

Epinephrine enhances glycogenolysis =

Raises Blood Sugar (makes new little sugars by breaking down stored
big sugars)
All of the above mentioned hormones are secreted during stress.
SOOOO
What happens to a persons blood sugar during stress?
What could this do to a borderline diabetic?
What about a diabetic who takes insulin?
 Vocabulary
commonly used terms
Hormones:

Insulin

Glucagon

Sugars

Glucose

Glycogen

Processes

Glycogenesis = glycogen + genesis

Gluconeogenesis = glucose + neo(new) +

genesis

Glycogenolysis = glycogen + lysis

Lipogenesis = lipo (fat) + genesis

Glycolysis= glucose + lysis

Carbohydrate Metabolism
Active transport of glucose into cells & metabolism (use) of glucose
with release of energy

Storage of glucose

Conversion of glycogen back to glucose

Conversion of proteins to glucose

CHO (cannot supply the bodys needs when:
When there is a decreased blood sugar &/or depleted glycogen
stores (starvation diets)

The cells are unable to use the available glucose

(D.M.)

When not enough CHO,

Body needs energy source
Catabolism of fats and proteins

Krebs Cycle!!!

Ketones (Acidic)

Diabetes Mellitus
Chronic disorder characterized by hyperglycemia

Imbalance between Insulin supply & demand

Abnormal metabolism of fat, carbohydrate, & protein

Statistics
Almost 6% of U.S. (16 million)
 7th leading cause of death

overall life expectancy by 1/3

Cost - $100 billion annually

Minority Populations

African-American twice the rate of white popn

Hispanics -- 3X the rate of white popn

Native Americans have highest incidence world-wide

50 - 75 % of all limb amputations

major cause of blindness

1/4 of all pts. on Dialysis -- DM

Unmeasured - loss of employment and ADL function

Types of DM
 *Type 1 (IDDM) 10 - 15 % of all Diabetics

*Type 2 85 - 90-% of all cases

Secondary

Gestational

(High Risk) Impaired Glucose Tolerance

Type l
(Type I)
IDDM = Insulin Dependent Diabetes Mellitus
Juvenile Diabetes

Body produces NO INSULIN

Must take at least one injection of insulin per day to
control blood sugar
Usually occurs before 30 years old
Body weight thin or ideal
Onset abrupt
TYPE 2
Type II
Adult/Maturity Onset
NIDDM = Non Insulin Dependent Diabetes Mellitus

Body does not produce enough insulin

 and/or

Body cannot use the insulin it has made

TYPE 2
Type II
Adult/Maturity Onset
NIDDM = Non Insulin Dependent Diabetes Mellitus

May control blood sugar with diet and exercise alone (but may take
oral meds. or insulin)

Clients usually > 35/40 years old

Clients usually overweight/obese

1/2 go undiagnosed for years & by then complications can be

underway

Four Cardinal Symptoms

Polyuria

Polydypsia

Polyphagia
 Weight Loss

WARNING SIGNS -TYPE 1

usually occur suddenly
3 polys & weight loss

irritability

weakness and fatigue

nausea and vomiting

WARNING SIGNS -TYPE 2

usually occur less suddenly & may be very mild

any of the Type 1 signs

recurring or hard-to-heal skin, gum or bladder infections

drowsiness

blurred vision

tingling or numbness in hands or feet

itching

RISK FACTORS
Heredity
Race

Increased Age

Obesity
 Stress

Viruses

Diet

Auto-immune

Environment

DM - Pathophysiology
Lack of Insulin

Glucose
Where?
ECF
 Fat & Protein breakdown

Ketosis & Negative Nitrogen balance

Hyperglycemia - - - WHY?

Intracellular fluid deficit

Glycosuria

ECF deficit

Signs of DM

Assessment - Lab Studies

FBS (>126 = DM)

(110-125 = impaired)

Postprandial glucose

Glycosylated Hgb (Hb A1c)(3 mo)

normal value is 3-8% (text says 6-7)
Assessment - Lab Studies
Glycolsylated Albumin - (1 week)

C-peptide(connecting peptide)

Proinsulin insulin

c-peptide

so c-peptide level indicates amount of insulin made

in the body (AKA endogenous insulin)

(Oral Glucose Tolerance Test =OGTT)

(Fractionals)

Ketonuria

Proteinuria

ICAs (Islet Cell Antibodies)-can detect diabetes in preclinical stages

FYI: Lab Study

ICAs (Islet Cell Antibodies)
1. Virus triggers autoimmune process

(beta cells destroyed)

2. ICAs present - Increase as more beta cells

destroyed

(80-90% destroyed before FBS increases!!)

3. Increased ICAs can predict/detect diabetes in

preclinical stages

(There are also insulin autoantibodies!)

Control
 Normal FBS - ACCUCHECKS

B.S. 180mg 2hrs. after a meal

Glycosylated Hgb 10% or less

Normal weight and general good health

Glucose Sensor
Placed under skin. It contains particles that give off light when glucose
levels increase. An external sensor, worn like a watch, monitors for
the changes in light and sounds an alarm to warn the client PRN.

Diabetes Management
Diet management

Physical Activity

Medications

Nutrition management
GOALS FOR MEDICAL NUTRITION THERAPY
1. Maintenance of near normal blood glucose.

2. Achievement of optimal serum lipid levels.

3. Adequate energy intake / reasonable body weight

 GOALS FOR MEDICAL NUTRITION THERAPY

4. Prevention of complications.

5. Improvement of overall health via optimal nutrition.

Recommended Nutrient Intake

PROTEIN 10 -20% of total energy intake

FAT < 30% (Depends on lipid

& glucose levels)

CARBOHYDRATE 40-60% of total intake (Based on

glucose & lipid levels and clients habits)

NCS

***FIBER*** 20-35 grams

Fiber slows/moderates blood absorption of carb/glucose

Example of Recommended Nutrient Intake

PROTEIN 15%

FAT 25%

CARBOHYDRATE 60%

6 MAJOR EXCHANGE LISTS

MILK Non-Fat, Low Fat

VEGETABLE All Non-Starchy Vegetables

FRUIT All Fruits & Fruit Juices

BREAD Bread, Cereal, Pasta,

Starchy Vegetables

& Prepared Foods

MEAT Lean Meat, Medium &

High Fat & Other

Protein Rich Food

FATS Polyunsaturated, Saturated

and Non Saturated

Medications
Type 1

Insulin
Administered SQ or IV NOT ORALLY
NOT IN TUBE FEEDINGS

Type 2

Oral Hypoglycemic Agents

Insulin

Insulin
Types of insulin

Duration of action
Short - Intermediate - Long
 Action
Onset - Peak - Duration

Insulin - (contd)
Concentration

Expressed in Units
U100

Insulin Order
NPH Humulin (U100) 32U SQ daily before dinner
 Types of Humulin Insulin and Comparative Actions
Special Things About Regular Insulin
Only one to give IV

Only one to give in Emergencies

Only one to give for coverage

Given via Insulin Pump (or Humalog)

Sliding Scale Insulin

Measure BG at -7am -11am - 4pm - 9pm

Give Humulin Regular Insulin

BG Value Dosage

150-200 0 units

201-250 2 units

251-300 4 units

301-350 6 units

351-400 8 units

over 400 call MD

under 50 give 6oz OJ

repeat BS

Insulin
 Dosage

Individual requirements

Individual response

Insulin Administration
Check Order

Gather equipment

Insulin - Precipitate

Administration - contd
Combining Insulins

30U of NPH & 6U of Regular

Drawing up

Nancy Reagan Registered Nurse

Injecting

NO aspiration - 900 angle not 450

Teaching
 Pathophysiology

Diet

Exercise

Diabetes Mellitus ID

Sexuality

Community Resources

Stress Management

Health Care

Teaching
Home management

Insulin
administration
storage
travel
exercise
sick days
Insulin pumps
Mimic release of pancreas

electro - mechanical with computer chip

Basal rate (++)

Sub-Q

Complications

Inhaled Insulin!!!
Complication of Insulin
Lipodystrophy

Atrophy

Hypertrophy

Cause

Management

FYI: Somogyi Effect

Overinsulinization- insulin rebound syndrome
 Normal defense Mechanisms

epinephrine, glucocorticoids, glucagon, ACTH

Blood sugar dramatically

Oral Hypoglycemic Agents

Use when:

Functioning Beta Cells

OOC on diet and exercise

Oral Hypoglycemic Agents
Sulfonylureas
All release insulin from beta cells

2nd gen. also enhance sensitivity of

receptor sites

1st gen = chlorpropamide (Diabinase)

2nd gen = glipizide (Glucotrol)

Oral Hypoglycemic Agents

 Biguanides

metformin - (Glucophage)
enhance sensitivity of receptor sites

Alpha-glucoside inhibitors

acarbose (Precose)
slows absorption of glucose

Oral Hypoglycemic Agents

Meglitinides

repaglinide (Prandin)
stimulates insulin secretion

Thiazolidinedones

rosiglinitazone (Avandia)
decreases insulin resistance and
increases insulin action

used to decrease amount of insulin or other

oral meds. For Type 2

(Insulin PRN)
Physical Activity
Exercise

Lowers BS levels

uptake of free fatty acids

lower cholesterol & triglycerides

promote cardiac stability

reduce stress & sense of well-being