Endocrine Disorders

Irma B. Ancheta, PhD, RNUniversity of North Florida

Endocrine“ductless” Lock and keyExcess production = hyperfunctionDecreased production = deficiency

Simple Negative Feedback Mechanism“ supply and demand”

Glucose insulin = maintain glucose levels

insulin (met) glucose

insulin

Complex Feedback Effect

• Look up this info• Glucocorticoids needed when stressed. Tells

hypothalamus… release C?H. Tells pit to release ACTH. Tells adrenals to release cortisol… adrenals then release the cortisol… From one gland to another gland.

hypothalamus

• Structure• A. hypothalamuic – hypophysial

– Portal system = allows hormones to travel from hypothalamus and APG

– B.

Pituitary Gland

Posterior Vasopressin (antidiuretic

hormone) = Kidney Oxytocin

Anterior (70% of all hormones produced here)

TSH (thyroid stimulating hormone)

ACTH LH FSH PRL (prolactin) GH MSH (melanocyte

stimulating hormone)

Adrenal Glands

Adrenal Cortex (outer layer)adrenal steroids or corticosteroids

90% OUTER layer (Glumerolosa) [1] mineralocorticosteroids (aldosterone, regulated by RAAS, ACTH) = [SALT] Na and water retention = K+ excretion MIDDLE Layer (Fasciculata) INNER layer (reticularis) [1] [SUGAR] Glucocorticosteroids (cortisol) [2] [SEX] Androgens [3] [SEX] Estrogens

Adrenal Medulla (inner layer)

Catecholamines [1] Epinephrine (85%) = Beta [2] NE (515%) =alpha receptors sitesSecreted in small amounts

at all times to maintain homeostasis

Addison’s Disease(Adrenal Gland Hypofunction)

Causes:[1] ACTH[2] dysfunction of hypothalic pituitary control

mechanism[3]dysfunction of adrenal gland tissue

Addison’s disease

Adrenal Cortex• Aldosterone

• Cortisol

Adrenal Medulla• catecholamines (E and NE)

Adrenal Cortex[1] Aldosterone (needed for Na and water retention/ K+ excretion)= K+ excretion is decreased hyperkalemia ?= Na and water NOT retained hyponatremia ? hypovolemia ?BP

Adrenal Cortex

[2] Decreased Cortisol levelsCan lead to gluconeogenesis hypoglycemiaHypoglycemia glomerular filtration gastric acid production Both of which urea nitrogen excretioncausing Anorexia Weight Loss

Adrenal Cortex

[3] Androgens = LevelsDecreased in body, axillary and pubic hair

growth

Diagnostic Labs

Addison’s Disease Cortisol = Decreased Aldosterone = Decreased[1] NA = ?[2] K+ = ?[3] Glu = ?[4] Ca = ?[5] BUN = ? Urinary 17hydroxycorticosteroids

(androgen metabolites) Skull x-rays (?), CT, MRI (pituitary) ACTH Stimulation test

Cushing’s Disease Cortisol = Increased Aldosterone = Increased [1] NA = ?[2] K+ = ?[3] Glu = ?[4] Ca = ?[5] BUN = ?

Intervention

[1] Fluid Balance (a) Weigh (b) I & O (c) monitor lab values (d) monitor for dysrthmmias[2] Cortisol/ Aldosterone Replacement(prednisone)/ (flurinef)

Treatment

[1] Primary Cause: (trauma, surgery, infection) (a) Cortisol and (b) aldosterone replacement

[2] Secondary causes: sudden cessation of high dose glucocorticoid therapy

Cushing’s Disease(Hypercortisolism)

Causes: [1] excessive stimulation/production of ACTH[2] excessive amounts of glucorticoids

Signs and symptoms

[1] increased glucorticoids= leads to hypergycemia carbohydrate metabolism increase in body fat (truncal obesity/ “buffalo

hump”) =kill lymphocytes, shrink organs containing

lymphocytes ( liver, spleen, lymph nodes) causing decreased

eosinophils, macrophages=leading to reduced inflammatory/ immune

responses

Signs and symptoms

[2] excessive androgens (sex hormone)= hirsutism and oligomenorrhea

• Cushing’s Disease= excess of cortisol,

secreted by adrenal gland (Endogenous)

= bilateral adrenal hyperplasia, Adrenal carcinomas

Cushing’s Syndrome= excess cortisol

(exogenous)= Use of ACTH or

glucoticoids (asthma, auto immune diseaases, organ transplantation,Ca chemo, allergic responses, chronic illness)

Cushing’s Disease General Appearance:[1] moon face[2] Buffalo hump[3] truncal obesity[4] Weight gainCV[1] HTN[2] dependent edemaMS[1] osteoporosis/pathologic fractureImmune system[1] Increased risk for infection[2] decreased lymphocytes[3] dcreased eosinophils

Diagnostic Assessment (Cushing’s Disease)

[1] check plasma cortisol levels[2] Check plasma ACTH(a) Ectopic = elevated(b) Primary cushings (from chronic steroid use)=low[3] Glucose = ?[4] Lymphocytes =?[5] Na = ?[6] Ca =?[7] K+ = ? 24 hour urine (17k , 17 h) 3 day low dose dexamethasone suppression test High dose dexamethasone suppression test

Nursing Diagnosis

[1] ?[2] ?[3] ?

The good thing is:= Cushing’s disease is RARE= Occurs 10 patients for every one million

Thyroid Disorders

Irma B. Ancheta, PhD, RNLinda Connelly, ARNP, MSN

A Thyroid Story

Management of patient with Thyroid disorders

Thyroid Gland• Butterfly shape• Hugs trachea• 2 lobes together

produce– T3 and T4

– Calcitonin

• T3 - triiodothyronine• T4 - thyroxine• Together Thyroid

hormone - body’s major metabolic hormone

• Calcitonin helps regulate blood calcium level by inhibiting the release of calcium from the bone

Thyroid Hormone

Regulation

TSH released from ant. Pituitary in response to TRH from the hypothalamus TSH stimulate the thyroid to produce T3 and T4 - iodine is crucial to this processCirculating T3 and T4 then exert negative effect on ant pit and hypothalamus to decrease production of TRH and TSHAll to maintain therapeutic level of T3 and T4 in the serum and stable metabolic processes in the body

Thyroid Hormone Effects on the Body

• Metabolism– Increase BMR - increase body heat production– Stimulate mobilize fat and enhance oxidation in

many tissues– Stimulates CHO and fat metabolizm

• Other effects– Increase HR, vasodilation, CO, contractility

Physiologic Effects of Thyroid HormonesIt is likely that all cells in the body are targets for thyroid hormones. While not strictly necessary for life, thyroid hormones have profound effects on many "big time" physiologic processes, such as development, growth and metabolism. Many of the effects of thyroid hormone have been delineated by study of deficiency and excess states, as discussed briefly below.

Diagnostic tests

• Serum Thyroid Antibody (TA)• Serum TSH• Serum T4

• Serum T3

• Radioactive Iodine Uptake• Serum Calcitonin

TA wnl negative to 1:20 ratioTSH> 1 m/l, T4 4.5 to 11.5 m/dl (microgram, mcg)T3 80-200 ng/dlRadioactive iodine 2hre 1-13%; 6 hrs 2-25%; 24 hrs 15-45%

Compare TSH with T4

Major thyroid disorders

• Hyperthyroidism– Grave’s Disease– Toxic Multinodular Goiter– Thyroiditis– Thyroid Storm

• Hypothyroidism– Iodine Deficiency– Hashimoto’s Thyroiditis– Myxedema Coma

Thyroid Disease StatesDisease is associated with both inadequate production and overproduction of thyroid hormones. Both types of disease are relatively common afflictions of man and animals.Hypothyroidism is the result from any condition that results in thyroid hormone deficiency. Two well-known examples include: ･ Iodine deficiency: Iodide is absolutely necessary for production of thyroid hormones; without adequate iodine intake, thyroid hormones cannot be synthesized. Historically, this problem was seen particularly in areas with iodine-deficient soils, and frank iodine deficiency has been virtually eliminated by iodine supplementation of salt.･ Primary thyroid disease: Inflammatory diseases of the thyroid that destroy parts of the gland are clearly an important cause of hypothyroidism.Common symptoms of hypothyroidism arising after early childhood include lethargy, fatigue, cold-intolerance, weakness, hair loss and reproductive failure. If these signs are severe, the clinical condition is called myxedema. In the case of iodide deficiency, the thyroid becomes inordinantly large and is called a goiter.

Hyperthyroidism

• Hypermetabolic condition with elevated T3 and T4

• Arises from many different factors– Autoimmune reactions (Graves)– Excess TSH from Anterior Pituitary– Thryoiditis– Neoplasms (multinodular goiter)– Excessive intake of thyroid medications

Grave’s Disease• Most common cause of hyperthyroidism (75% of cases)• 5 times more prevalent in women than men• Occurs most frequently between 20 and 40 years of age• Seen worldwide, incidence correlated with amount of

iodine in diet• Precipitated by stress, infections, genetic factors

Clinical Manifestations

EXOPHTHALMOS GOITER

Exophthalmos • Impaired drainage from orbit, increasing fat and edema in retroorbital tissues

• Eyeballs forced outward and protrude

• Corneal surfaces become dry and irritated

Toxic Multinodular Goiter

• Slower to develop than Grave’s disease

• Multiple nodules in the thyroid secrete excessive amounts of TH

• Usually women 60-70 years of age

• Characteristic massive enlargement of neck (goiter)

Thyroid Storm• Life threatening condition• Precipitated by severe illness

or injury, or surgical manipulation of thyroid

• Rapid increase in metabolic rate

• Hyperthermia up to 106 deg. F, respiratory distress, tachycardia, hypertension, severe GI symptoms, confusion, delirium, coma

• High mortality rate

Diagnostic Studies

Primary hyperthyroidism• T3 and T4 elevated• TSH suppressed• Radioactive iodine uptake is increased in

Graves' disease

Hyperthyroidism: goals and treatment

• Goals– Reduce production of TH– Establish euthyroid state– Prevent and/or treat complications

• Collaborative treatment– Medications– Radioactive iodine therapy– Surgery

Pharmacologic therapy antithyroid medications

• Potassium iodide (SSKI, Thyro-Block)– CHECK ALLERGIES to shellfish– Bleeding precautions– Bitter taste - give with OJ– Maximum effect in 2 weeks

• Tapazole, Propylthiouracil– Monitor for s/s hypothyroidism especially if taking

lithium– Bleeding precautions– Effects may take up to 12 weeks

SSKI - Inhibits TH synthesis and releaseHyperplastic thyroid less vascular before surgeryHastens ability of other antithyroid drugs to reduce natural hormone outputPTU inhibits TH production only

Radioactive iodine therapy

• Measured dose given orally• Results in 6-8 weeks• 131I concentrates in thyroid

cells and damages them so they produce less TH

• TAKEN AT HOME, NO RADIATION PRECAUTIONS NEEDED

• Contraindicated in pregnant women

Surgery: thyroidectomy

• Subtotal thyroidectomy indicated when thyroid pressing on trachea– leaves enough gland to produce TH

• Total thyroidectomy primarily for cancer of the thyroid– Requires lifelong hormone replacement

• Endoscopic thyroidectomy appropriate with small nodules with no malignancy– Less scarring, pain, and recovery time

Breathing or swallowing problemsSubtotal thyroidectomy involves removal of significant portion of thyroid

90% removed to be effectiveIf too much is removed, regeneration will not occur, results in hypothyroidismSurgical Therapy

Indicated for those unresponsive to drug therapy with large goiters causing tracheal compression with possible malignancy

Peri-operative care• Pre-op

– Euthyroid preop– Antithyroid meds, Iodides to reduce

hemorrhage risk• Post-op

– Semifowler’s position – Support head and neck to decrease strain on

suture line– High risk for hemorrhage - check behind head

and neck– Risk for respiratory distress - have suction at

bedside and intubation equipment readily available

– Tetany - check for signs of calcium deficiency

Hemorrhage - vascularity, positioning - blood drains behind - don’t seeResp - hemorrhage and edema, tetany and laryngeal spasmsTETany - can be damage to parathyroid glands

Hypothyroidism

• Results when thyroid gland produces insufficient TH decreasing metabolic rate and heat production

• Effect of antithyroid drugs• One of the most common medical disorders in the U.S.• Affects 8% of women • Affects 2% of men over 50• Hypothyroidism associated with high incidence of

depression, especially in women

Etiology

• Primary hypothyroidism– Congenital defects in the gland (Cretinism)– Loss of thyroid tissue from

• Surgery• antithyroid medications• Endemic iodine decifiency• Thyroiditis

• Secondary hypothyroidism– Pituitary TSH deficiency– Goitrogenic drugs– Peripheral resistance to TH hormones

Slow onset, manifestations appearing over months or years, rapidly reverses with treatmentGoitrogenic drugs: lithium, antithyroid drugs, - block TH synthesisAs TH decreases gland enlarges to conpensate - simple or nontoxic goiter

Iodine Deficiency Hypothryoidism

• Iodine needed for TH synthesis

• Thyroid gland enlarges in its attempt to make up for this deficit

• Simple non-toxic goiter• Rare in U.S. due to use of

iodized salt

Hypothyroidism

Iodine deficiency is the most common cause worldwide and is most prevalent in iodine-deficient areasIn places where iodine intake is adequate, the primary cause in the adult is atrophy of the gland

Iodine deficiency is the single most common cause of preventable mental retardation and brain damage in the world. It also decreases child survival, causes goiters, and impairs growth and development. Iodine deficiency in pregnant women causes miscarriages, stillbirths, and other complications. Children with IDD can grow up stunted, apathetic, mentally retarded, and incapable of normal movements, speech, or hearing. Globally, 2.2 billion people (38% of the world's population) live in areas with iodine deficiency and risks its complications.Iodine deficiency was once considered a minor problem, causing goiter, an unsightly but seemingly benign cosmetic blemish. However, it is now known that the effects on the developing brain are much more deadly, and constitute a threat to the social and economic development of many countries.Effective and affordable technology exists to prevent iodine deficiency and the problems it causes. The most important are iodized salt and effective monitoring of iodine nutrition.

Cretinism

• The most severe and devastating form of hypothyroidism

• Congenital hypothyroidism is inadequate thyroid hormone production in newborn infants.

• Can progress to cretinism, a form of irreversible growth and mental retardation.

Congenital hypothyroidism is inadequate thyroid hormone production in newborn infants. This can occur because of an anatomic defect in the gland, an inborn error of thyroid metabolism, or iodine deficiency.The term endemic cretinism was initially used to describe clusters of infants with goiter and cretinism in defined geographic areas. Eventually, these areas were discovered to be low in iodine, and the cause of endemic cretinism was determined to be hypothyroidism secondary to iodine deficiency. In the 1930s, adequate dietary intake of iodine was found to prevent this goiter and cretinism. Thus, the wholesale iodization of salt was established. In spite of its efforts, the World Health Organization (WHO) has not been able to eliminate iodine deficiency completely throughout the world. As a result, endemic goiter and cretinism are still observed in some isolated areas, such as regions of Bangladesh, Chad, China, Indonesia, Nepal, Peru, and Zaire.

Cretinism

Hashimoto’s Thyroiditis

• Most common– Primarily in women– Familial link

• Autoimmune disease• Goiter comes and goes

Antibodies develop that destroy thyroid tissue and replace with fibrous tissueGland enlarges in early phases to compensate - goiterGland shrinks as disease progresses

Myxedema Coma

• Life-threatening complication of untreated hypothyroidism

• Severe metabolic disorders, hypothermia, cardiovascular collapse, coma

• Rare• Precipitated by trauma, infection, failure to take meds,

CNS depressants, exposure to cold• (Metabolic disorders - low sodium, glucose, lactic

acidosis• Older women in winter with longstanding disease)

Diagnostic Studies

• Diagnosed with decreased TH, particularly T4

• TSH increased in primary hypothyroidism• TA normal• (TSH up due to loss of negative feedback to

anterior pit)

Management of Hypothryoidism

• Goal– Diagnosis, prevention and treatment of

complications– Replacement of deficient TH

• Therapy– Medications– Surgery– Other preventive treatments

Medications

• Thyroid preparations– Levothyroxine sodium– Liothyronine sodium

• Teach to take one hour before breakfast• Potentiates effects of anticoagulants and

digoxin

Insomnia and GI absorptionRaise blood levels of TH therefore raising metabolic rateIncreased cardiac output, oxygen comsumption and body temperatureMonitor for s/s digoxi toxicityMonitor for coronary insufficiency, chest pain, dyspnea, tachycardiaEffects of insulin may change as thyroid function increases – take pulse before administering and report > 100Do not switch from brand to generic or back

Medication Administration

• Report symptoms of hypo and hyper thyroid• LIFELONG CARE• Watch BG closely• Increased risk for iodine toxicity, bleeding, dig

toxicity, changes in menstrual periods• Avoid excessive intake of TH inhibiting foods

– Turnips, cabbage, carrots, spinach, peaches

Surgery for Hypothyroidism

• Thyroidectomy for goiter large enough to cause – Respiratory difficulties– Swallowing problems

Nursing care for a slow body

• Decreased cardiac output• Constipation• Risk for impaired skin integrity• Mood changes• TH dec – reduced HR and stroke volume - hypotension; edema cn

be expressed as pericardial fluid (restricts heart function)• Decreased appetite, decreased food intake, decreased activity

levelreduced peristalsis• Hypo causes dry, rough, edematous skin conditions

Diabetes: Nursing Care and Education

Linda Connelly, ARNP, MSNIrma B. Ancheta, PhD, RN

DIABETIC EDUCATION:

Demonstrate accurate blood glucose monitoring

• Work with M.D. and Diabetic Educator• Assess patient and support system to recommend appropriate

machine– What insurance will allow– Test on finger or arm?– Size of blood drop needed?– Long-term or short term?– Get Rx as needed

• Patient and family to obtain supplies• Teach all who will be doing and have others observe if possible• SW can help with supplies for testing and injection

Demonstrate accurate insulin administration

• Work with M.D. and Diabetic Educator• Assess patient and support system to

recommend appropriate delivery devices– Syringe, pen, pump, etc.– BG machine – complexity, cost, amount of blood needed– Get Rx as needed and check funding

• Promote self-care– Patient and family to obtain supplies

• Determine and teach all who will be giving the insulin and, if the patient cannot, who can be a backup support– Include universal precautions and disposal of sharps at home

Identify s/s hypoglycemia and take proper actions

• Teach family s/s, causes, prevention, treatment

• Wear or carry identification• May or may not be

symptomatic– Take BG if have symptoms

• Ingest 15 grams rapid acting sugar (Keep simple CHO with you at all times)

• 15/15 rule– Wait 15 min and recheck BG – Repeat 15 gram snack if still

low– Repeat until normal if mild

Rapid acting sugar3 glucose tabs8 oz skim milkFive lifesavers, ½ cup fruit juice or

reg. sodaFBS - effect of PM intermediate

insulinBefore lunch - effect of A.M. short-

acting insulinBefore supper - effect of A.M.

intermediate insulinBedtime - effect of P.M. regular

insulin

Identify s/s hypoglycemia and take proper actions – severe

• For BG < 50, coma, seizures, altered behavior• No response after 12 hours of 15/15• Oral CHO is conscious and alert• IV glucose if decreased LOC

– glucagon

Develop a plan for sick day management

• Continue usual dose of insulin or oral agents• Force fluids• Maintain caloric intake as scheduled if possible• If unable to eat, replace with clear liquids• Test blood glucose frequently and adjust diet and

insulin accordingly• Call PCP for

– sustained BG over 300mg/dl – Persistent nausea, vomiting, fever, diarrhea– S/S infection - urine, skin, etc.

• Management with frequents checks and regular insulin for surgery

Explain that stress and ilness increase blood sugar - can be high without eating

Diabetic Foot Care• Inspect daily, palpation for

vision impaired• Bathe feet qd mild soap & water• Check water temperature• Dry thoroughly and apply lotion

or cream• DO NOT SOAK• Podiatrist for problems

• Prone to foot ulcers due to decreased peripheral sensation and circulation .

Demonstrate appropriate foot care

• Cotton socks• Beware of new shoes• Diabetic shoes• No flip flops!• Don’t go barefoot

Identify the causes and prevention of long-term complications

• Heart disease is the leading cause of death for people with diabetes.

• Adults with diabetes should have yearly eye exams to ensure the health of their eyes and to protect their vision.

Three out of four diabetes-related deaths are caused by heart and blood vessel (cardiovascular) disease. People with diabetes are 2-4 times more likely to have heart disease than persons without diabetes. Even people with type 2 diabetes who do not have heart disease have an increased risk of having a heart attack. People with diabetes also tend to have other risk factors for heart disease including obesity, high blood pressure, and hardening of the arteries (atherosclerosis).In recent years, FDA has approved drugs that lower blood pressure and reduce the risk of heart attacks and strokes. It has also approved lipid-altering drugs that target abnormalities of cholesterol and triglycerides.Over time, high blood sugar levels can damage the blood vessels that feed the retina of the eye. In nonproliferative diabetic retinopathy (NPDR), an early stage of diabetic eye disease, the blood vessels may leak fluid. This may cause the retina to swell and vision to blur, a condition called diabetic macular edema. In advanced or proliferative diabetic retinopathy (PDR), abnormal new blood vessels grow on the surface of the retina. The abnormal blood vessels don't supply the retina with normal blood flow. In addition, they may eventually pull on the retina and cause it to detach. Some cases of diabetic retinopathy can be treated with laser surgery. In this procedure, doctors aim a strong beam of light onto the patient's retina to shrink or seal leaking or abnormal vessels. Laser surgery can't restore vision already lost, so early detection is important. In some advanced cases of PDR, a surgeon may remove the vitreous portion of the eye and replace it with a clear solution (called a vitrectomy).

Identify the causes and prevention of long-term complications

• Over time, high blood sugar levels can damage the kidneys.

• Adults with diabetes need to take special care of their feet.

Healthy kidneys act like filters to clean the blood of waste products and extra fluid. Damaged kidneys do not clean the blood well. Instead, waste products and fluid build up in the blood. People with kidney failure must either have dialysis treatment (to substitute for some of the filtering functions of the kidneys) or receive a kidney transplant. FDA regulates dialysis equipment. The agency does not inspect dialysis clinics--that is the responsibility of each state health department--but FDA approves the equipment used in dialysis. Recently, the agency has begun requiring that hemodialyzer filters and tubes be tested and approved in realistic clinical situations. For example, in about eight out of 10 hemodialysis treatments, the equipment is reused to cut costs, although it was originally tested, labeled and approved for one-time use only. FDA is now requiring manufacturers to prove that filters and tubes are safe and effective when reused. FDA is also taking a closer look at water purifying equipment used in dialysis. Pure water is crucial to hemodialysis, since impurities can kill a patient. FDA has recently begun enforcing regulations that require the manufacturers of water purifiers to prove their devices are safe and effective.

People with diabetes are at risk for foot injuries due to numbness caused by nerve damage (diabetic neuropathy) and low blood flow to the legs and feet. The most serious injury is a foot ulcer. Diabetic foot ulcers are at very high risk of becoming infected, and sometimes they cannot be healed. Non-healing foot ulcers are a frequent cause of amputation in people with diabetes. Patients with foot ulcers may use wound dressings, skin substitutes, or other treatments to protect and heal their skin.Wound dressings are medical devices that are used to protect ulcerated skin and assist in its healing. They can range from simple bandages that you can buy in the drug store to complex materials that contain antibacterial and antiviral substances. Skin substitutes are products that help in closing the wounds of slow healing ulcers in patients with diabetes. They are made from human cells known as fibroblasts that are placed on a dissolvable mesh material. When the mesh material is placed on the ulcer, it is gradually absorbed and the human cells grow and replace the damaged tissue in the ulcer. FDA has cleared one gel product (becaplermin) that is used as a treatment for diabetic foot ulcers. This product contains genetically engineered platelet-derived growth factor, one of the proteins the body produces to encourage new tissue growth. Clinical studies of the product indicated that the likelihood of complete ulcer closure, after up to 20 weeks of treatment, was greater when becaplermin is used.

Diabetic Education:Identify the rationale for exercise and the effect on glycemic control – Type I

• Keep exercise moderate and regular– Low-impact aerobic recommended

• Hyperglycemia may be associated with brief, intense exercise

• Hypoglycemia may be associated with prolonged exercise or exercising at peak insulin action time

• Check BG before and after

Diabetic Education:Identify the rationale for exercise

and the effect on glycemic control – Type II

• Check-up to discover complications first• Begin slow with mild exercises and

gradually increase intensity and duration• Check BG before and after• Include muscle-strengthening and low-

impact aerobic exercises

Demonstrate meal planning within orders• Work with R.D.• Match foods with peak insulin action times• Food = Culture

– Individualized mealtimes need to fit family routines and preferences

• Observe the home for food – look in the fridge• http

://www.diabetes.org/all-about-diabetes/chan_eng/i3/i3dm.htm

• http://www.ndep.nih.gov/• Match mealtime with peak action time – 3 well-spaced

meals plus daily evening snack• Describing the diabetes disease process and treatment

options

Diabetic Education

• Involves entire household to include as many as possible

• Cannot manage without access to healthy food, medication, and devices

• Do not assume that they are experts because the patient has had Diabetes many months or years

• Do not assume they are doing what they say

• Teach –Teach-Teach!!