Endocrine System: diseases of the Pancreas

PN 1V

Winter 2008

What is Diabetes?

• A person’s blood sugar levels are too high • Type 1: Pancreas produces little to no insulin• Type 2: Over time, lose ability to use the insulin

that the body makes

Pizza

Blood sugar

Insulin

Blood sugar

Who has Diabetes?• About 7% of the population (21 million people)

had diabetes in 2005 (2)• Type 1:

– Usually diagnosed in children and young adults – About 5-10% of people with diabetes have type 1

• Type 2:– Older Adults Children, adults, and older adults!!!– About 90-95% of people with diabetes have type 2

diabetes

What are the risk factors for type 2 diabetes?

• Age• Physical inactivity• Being overweight• For women:

gestational diabetes• Some racial/or ethnic

groups • Type 2 diabetes in the

family

How Bad is Type 2 Diabetes, Really?

• Increases your risk of….– Heart disease, high

blood pressure and stroke by about two times.

– Other complications include blindness, numbness, amputation, impotence, and kidney failure!

The Risk Triangle: A Type 2 Diabetes Example

Your Genetics

Your Behavior

Your Environment

Your Risk

Using Family History for Prevention

• Environment and behavior are modifiable risk factors

• Genetic make-up is a non-modifiable risk factor

• You can prevent disease by changing modifiable risk factors

Genetics

Behavior

Environment

Risk Risk Risk

Diabetes Mellitus (DM)

• Disorder of the pancreas characterized by insufficient or absolute lack of insulin production causing hyperglycemia, requiring life-long lifestyle adjustments and resulting in multisystem changes in health status (clients with DM have a 2-4% > chance of heart disease, 2-6% > incidence of stroke/CVA, increase in blindness, nontraumatic amputation, renal failure)

DM

• Affect about 4-6% of the population and fourth leading cause of death

• Type 1: auto immune destruction of the beta cell; genetic predisposition, more common in men, can occur at any age but usually in children and adolescents; characterized by hyperglycemia and ketosis

DM

• Type 2: exact cause unknown, could be compromised ability if beta cells to respond to hyperglycemia, or abnormal insulin receptors on the cells, or peripheral insulin resistance

• Genetic predisposition, can occur at any age, more common in obese, older adults, African-Canadians, Hispanic-Canadians, Native Canadians, now becoming common in children

DM

• Symptoms (refer to hand out)

• Diagnostic tests: – Elevated random and or fasting bld glucose,

possible positive serum ketones, elevated glycosylated hemoglobin, abnormal oral GTT, urine positive for glucose, and possible positive ketones or acetone.

How Can We Treat and Prevent Type 2 Diabetes?

• Treatments:– Medications– Lifestyle changes

Prevention:– Learn about your family history– Work with doctor to monitor health closely, if it

runs in family– Eat a healthy diet and be physically active!

Therapeutic Management

• Food (Diet is a bad word!)

• Oral antidiabetic meds

• Insulin therapy

• Exercise

Hypoglycemic reaction

Mild Moderate Severe

Blood glucose

<4 <4 <2.8

Symptoms Autonomic Autonomic & neuroglycopenic

Autonomic and neuorglycopenic +/- seizures, unconscious

Ability to tx Able to tx self

Able to tx self

Requires assistance

Tx goals

• Detect and tx low BS quickly

• Relieve symptoms quickly, avoid rebound or over treatment

Rule of 15

• Observe pt consume 15 gms carbs

• Repeat BS in 15 mins

• Repeat tx every 15 mins prn (max 3) until BS is >4

• * do not delay treatment but notifiy MD if initial bld sugar remains <4

• Provide pt with next meal, or 15 gms carb and a protein if meal is > 1 hour away

Alternate tx

• Enteral access (50% dextrose)

• Parenteral access (50% dextrose)

• IM treatment (glucagon)

Recommendations for Kids

• Children > 5 oral tx same as adults

• Children < 5 10 grms of fast acting carb not 15

Control is Based on Balance

Food

Meds Activity

Food

• Carbohydrates = blood sugar, 50=60% of calories should come from carbs

• Food intake affected by; lifestyle, NPO, fluid diet, poor intake, vomiting, enteral feeds and TPN

• Danger when intake is interrupted but meds are given

• 50 to 80 gms intake at each meal

Each Meal

• 1 choice of

• Starch (15 gms carb)

• Fruit & sweet veg (10 grms carb)

• Milk (6 grams carb)

• Sugar (10 grms carb)

• Protein, fats, extras (low in carbs)

Sample Lunch

• 6 oz soup = 15

• 1 sandwich = 30

• 125ml milk=6

• 125ml applesauce=10

• Lettuce salade(dsg) tea = minimal

• Total: 61 gms

Food (clear & full liquids)

• Approx 200gms of carbs/day divided into 3 meals and 3 snacks i.e reg gingerale, juice, jello

• Sugar free fluids maintain hydration but do not add carbs!!!

• Progress from liquid to solid diet quickly as possible

Food (Diet)

• Hypoglycemic reaction

• Food (Diet is a bad word)

• Illness

• Glucometer use

Oral Antihyperglycemics

• Insulin Secretogogues:

• Stimulate pancreas to produce more insulin; glybride, Amaryl, Diabinese

• **can cause hypoglycemia

• Glybride may continue to stimulate pancreas up to 24 hours

• Patients over 6o are especially sensitive

Oral Antihyperglycemics

• Biguanides (Metformin)

• Work on the liver to decrease glucose output

• Helps insulin resistance at the cell level

• May suppress appetite

• Contraindicated in kidney & liver disease, CHF

Oral Antihyperglycemics

• Thiazolidinodiones (TZD”S): Avanda

• Decreases insulin resistance at the cell level and increases glucose uptake by the cells

• Contraindicated in CHF

Oral Antihyperglycemics

• Alpha Glucosidase Inhibitors: Prandase

• Slows absorption of starch and sucrose in gut

• In combination therapy, hypoglycemia can not be treated with food, must be glucose tabs

Oral Antihyperglycemics

• Combination Meds:

• Glybride+metformin

• Glybride+ metformin+TZD

• Glybride+Metformin+TZD+ HS insulin

• Insulin, Metformin and/or TZD

• Tx goal = BS in range of 4 to 7

Polypharmacy

• Glucose control

• Cholesterol control

• BP control

• Neuropathy drugs

• ASA

• Non-diabetic meds

Insulin

• Hormone produced by pancreas• Controls the livers production of sugar• Insulin without adequate nutrition causes

hypoglycemia• Refer to your pharm notes regarding onset

of insulin.• Never give until trays are on floor.• Always check that pt has eaten food and

snack

Exercise

• Exercise can cause hypoglycemia in people on insulin secretagogues or insulin

• Risk may last many hours after exercise

• Inactivity may be cause hyperglycemia

• What safety teaching would you provide to someone taking part in physical activity?

Nsg Diagnosis

• Ineffective individual coping

• Ineffective health maintenance

• Risk for infection

• Risk for impaired skin integrity

• Risk for injury

• Risk for disturbed body image

• Knowledge deficit

hyperglycemia

• Extra food or drink• stress./illness/surgery• Not rotating sites for injection• Spoiled insulin• Not enough pills/insulin• Decreased activity• Weight gain• Glucometer inaccuracy

Blood glucose Monitoring

• “vital sign”

• Recommended times fasting and/or AC meals and/or 2 hours

• Test at varying time of the day to best determine the effectiveness of mediations/insulin and effects of food/activity on glycemic control.

Diabetic Ketoacidosis (DKA)

• Life threatening metabolic acidosis resulting from persistent hyperglycemia and breakdown of fats into glucose, leading to presence of ketones in the blood; can be triggered by emotional stress, uncompensated exercise, infection, trauma, insufficient or delayed insulin administration

Etiology

• Hyperglycemia causes uncompensated polyuria, hemoconcentration, dehydration, hyperosmolarity and electrolyte imbalance; a significant accumulation of serum ketones leads to acidosis

Manifestations

• Thirst, nausea, vomiting, malaise, lethargy, polyuria, warm dry skin, flushed face, acetone odor to breath, Kussmaul respirations (deep, nonlabored, rapid)

Diagnostic findings

• Serum glucose

• Plasma pH <7.35

• Plasma bicarb <15mEq/L

• Serum ketones present

• Urine positive for glucose and ketones;

• May have abnormal serum sodium and chloride levels and hyperkalemia

Treatment

• IV fluids, electrolytes, regular insulin

• Supportive care possibly NPO, vasopressors and ventilator to support respirations

• Insulin, Fluid therapy, K+ replacement,

• Frequent BS

Hyperglycemic hyperosmolar nonketotic coma (HHNK)

• Life threatening metabolic disorder of hyperglycemia usually occurs with DM2 and triggered by a variety of situations such as medications, infection, acute illness, invasive procedure, or chronic illness

Etiology

• Increased insulin resistance (caused by one or more of the triggering situations) along with increased carb intake leads to hyperglycemia, followed by polyuria, decreased plasma volume, decreased glomerular filtration rate leading to glucose retention and Na and water excretion; hyperosmolarity causes dehydration and reduced intracellualr water (cell shrinkage)

Manifestations

• Symptoms gradually occur over 24 hours to 2 weeks and include; decreased LOC, dry MM, polydipsia, hyperthermia, impaired sensory and motor function, positive Babinski sign, and seizures

• Elevated Na, serum osm>340, BS> ,

• Abn K+ and chloride

• No ketones and normal serum pH

Treatment

• Correct triggering situation

• Treat co-exisiting health deviations

• Provide fluid and electrolytes replacement

• Regular insulin IV