St. Louis Review CenterIligan City

Name:

Endocrine DisordersPrepared by: Roquee Hospicio H. Paragoso, RN

I. The Endocrine Systema. Second great controlling system of the bodyb. Small and unimpressive organs yet with a very impressive function: to

maintain body homeostasisc. Both the nervous and immune systems interact closely with this

systemd. Hormones (from Greek word meaning “to arouse”) – chemical

substances, secreted by cells into the extracellular fluids, that regulate the metabolic activity of other cells in the body.

II. Classification and Action of Hormonesa. Steroid – penetrates the cell membranes and interact with intracellular

receptors b. Amino acid-based – interact with receptor sites on the cell surface

III. Control of Hormone Release a. Negative Feedback Mechanisms

i. Hormonal Stimulus- most common- endocrine organs are prodded into action by other

hormones- “One goes up the other goes down”

ii. Humoral Stimulus- Changing blood levels of certain ions and nutrients serve

as stimuli for hormone release

iii. Neural Stimulus- Stimulation by nerve fibers

IV. Major Endocrine Organs1. Pituitary gland

- Anterior pituitarya. Growth hormone (GH) – promotes total body growthb. Prolactin (PRL) – production of breast milkc. Adrenocorticotropic hormone (ACTH) – stimulates adrenal

cortex to release its hormonesd. Thyroid-stimulating hormone (TSH) – stimulates thyroid gland

to release its hormonese. Gonadotropic hormones

i. Follicle-stimulating hormone (FSH) – stimulates follicle development and estrogen production in females; sperm production in malesii. Luteinizing hormone (LH) – stimulates ovulation, converts follicle to corpus luteum and causes eventual production of progesterone; stimulates male’s testes to produce testosterone

- Posterior pituitarya. Oxytocin – stimulates powerful uterine contraction

and causes milk ejectionb. Antidiuretic hormone (ADH) – causes kidney tubules

to reabsorb and conserve body water and increase BP by constricting blood vessels

2. Thyroid glanda. Thyroid hormones (Thyroxine [T4] and triiodothyronine [T3])

– body’s metabolic hormonesb. Calcitonin – released as a response to high serum calcium

levels; causes calcium reabsorption of the bones

3. Parathyroid glanda. Parathyroid hormone (PTH) – released as a response to low

serum calcium levels; causes liberation of calcium from the bones into the blood

4. Adrenal gland- Adrenal cortex

a. Mineralocorticoids – primarily aldosterone; regulate Na and K ion reabsorption by the kidneys

b. Glucocorticoids – enables body to resist long-term stress by increasing blood glucose levels and depressing inflammatory response

c. Sex hormones – (mainly male sex hormones) are produced in small amounts throughout life

- Adrenal medullaa. Catecholamines (epinephrine and norepinephrine) –

released in response to SNS stimulation enhancing or prolonging the effects of the fight-or-flight response to short-term stress

5. Pancreatic isletsa. Insulin – released by the B-cells of the Islets of Langerhans as

a response to high serum glucose levels increasing the rate of glucose uptake and metabolism by body cells

b. Glucagon – released by the A-cells of the Islets of Langerhans as a response to low serum glucose levels stimulating the liver to release glucose to blood

6. Pineal gland – releases melatonin which affects biological rhythms and reproductive behavior

7. Thymus gland – its hormone, thymosin, promotes maturation of T lymphocytes, important in body defense

8. Gonads- Ovaries

a. Estrogens – influenced by FSH, they stimulate maturation of the female reproductive organs and development of secondary sex characteristics of the female.

b. Progesterone – influenced by LH, released from the corpus luteum and works with estrogen to establish the menstrual cycle

- Testesa. Testosterone – influenced by LH, promotes maturation of the

male reproductive organs, male secondary sex characteristics and production of sperm by the testes

V. Common Diseases of the Endocrine System

HYPERTHYROIDISM - Also known as Grave’s Disorder, Parry’s Disorder,

Exopthalmic Goiter, Toxic Diffuse Goiter, Thyrotoxicosis- Commonly occurs in women below 40 years of age, after

severe emotional stress and as a result of an autoimmune disorder (Hashimoto’s disease)

Simple Pathophysiology Hyperactivity of the thyroid gland would cause an increased production of the thyroid hormones thus increasing metabolic rate (T3), increasing body temperature (T4) and causing hypocalcemia (calcitonin).

Assessment Findingsa. Heat intoleranceb. Tachycardiac. Hypertensiond. Weight losse. Increased appetitef. Diarrheag. Diaphoresish. Restlessness, nervousness, irritability, agitationi. Amenorrheaj. Fine tremorsk. Fine silky hairl. Opthalmopathy

Exopthalmos – due to the accumulation of fluids at the fatpads behind the eyeballs, pushing the eyeballs forward

Lid Lag (Von Graefe’s Sign) – Long and deep palpebral fissure is still evident when one looks down

Jeffrey’s Sign – Forehead remains smooth when one looks up

Thyroid Stare (Dalyrimple’s Sign) – bright-eyed stare, infrequent blinking

Diagnosticsa. Palpation and Auscultation of the Thyroid Gland

- The isthmus is the only portion of the thyroid that is normally palpable unless the patient is very thin- Auscultation (to check for bruit) follows when the thyroid is enlarged upon palpation

b. Thyroid-Stimulating Hormone- Single, best screening test of thyroid function in outpatients because of its high sensitivity- Values above 0.4-6.15 μU/ml: primary hypothyroidism; below the normal: hyperthyroidism

c. T3 and T4 levels (if both are increased, hyperthyroidism; if both are decreased, hypothyroidism)

d. PBI (protein-bound iodine)- No foods, drugs, test dyes containing iodine 7-10 days prior the test

Partial List of Medications That May Alter Thyroid Test Results:

Estrogens Chloral HydratePropylthiouracil

Sulfonylureas X-ray contrast agentsCorticosteroids Opiates Iodine AndrogensPropranolol ClofibrateCimetidine Furosemide5-Fluorouracil DiazepamPhenytoin DanazolHeparin Dopamine antagonists

e. Radioactive Iodine Uptake- oral intake of a tracer dose of I131

- Exposure to scintillation camera for 2°, 6° and 24°- No foods, drugs, and test dyes with iodine, as well as oral contraceptive pills 7-10 days prior to the test- Increased uptake, hyperthyroidism; Decreased uptake, hypothyroidism

f. Thyroid Scan- Patient is given an radioisotope per IV and then exposed to a scintillation camera

g. Fine Needle Biopsy- assesses malignant growth in the thyroid gland

h. Basal Metabolic Rate- measures O2 consumption at the lowest cellular activity- Procedures:

NPO 10-12° before the procedure Get a good night’s sleep of 8-10° Do not get up from bed the following morning until

the test is finished A device with a noseclip and a mouthpiece is used;

the client is then asked to perform deep breathing exercises Normal: ± 20% (euthyroid state)

Nursing ManagementTo address manifestations:

a. Provide a non-stimulating cool environment to promote restb. ↑ calorie, protein, vitamin and mineral supplementsc. ↓ fibers if diarrhea is present and avoid stimulantsd. Promote safetye. Protect the eyes – give artificial tears at regular intervals and

encourage to wear sunglasses when going out under the sun.f. Replace fluid-electrolyte losses as ordered.

Medical Managementa. Medications

Beta-blockers (Inderal) – to control tachycardia and hypertension Potassium Iodide Saturated Solution (KISS or Lugol’s Solution) –

to inhibit release of thyroid hormone- Mix with icy fruit juice or cold glass of water to improve taste- Use drinking straw to prevent permanent staining of teeth- Monitor for allergic reactions, increased salivation and coryza

Propylthiouracil (PTU) and Tapazole (Methimazole) – inhibit synthesis of thyroid hormone by interfering with the iodination of thyrosine and the coupling of iodothyrosines

- Monitor for fever, sore throat and rashes (S/S of Agranulocytosis and Neutropenia)

Calcium-channel blockers Thyroid hormones (Levothyroxine sodium [Synthroid] and

Thyroglobulin [Proloid]) – puts the thyroid gland at rest. These are slow-acting drugs and usually take about 10 days to take effect.

b. Radiation Therapy- Radiation with I131

- DTS still applies. Isolation for few days; Body secretions are radioactive.

- Do not use in pregnant women because of its teratogenic effects. Delay pregnancy for 6 months post-therapyc. Surgery

Subtotal Thyroidectomy- 5/6 of the thyroid gland is removed - reserved for special circumstances: pregnant women allergic to antithyroid medications, patients with large goiters or patients unable to take antithyroid agents- performed soon after achievement of euthyroid state within 4-6 weeks of therapy

PREOP CARE1. Promote euthyroid state2. Administer iodides as ordered – reduces the size and

vascularity of the thyroid gland thereby preventing post-op hemorrhage and consequent thyroid crisis

3. Monitor ECG – prolonged hypertension and tachycardia often results to heart failure or cardiac damage

POSTOP CARE1. Semi-Fowler’s position with head, neck and

shoulder erect.2. Prevent hemorrhage – place ice collar over

neck. ALWAYS CHECK BACK OF NECK for blood.3. Keep tracheostomy set available for the first

48° postoperatively – hypocalcemia as a result of parathyroid damage causes laryngospasm and consequent airway obstruction

4. Encourage to speak every hour upon return of consciousness – to assess for laryngeal nerve damage

5. Ca gluconate at bedside – calcium replacement when hypocalcemia develops

6. Monitor body temperature – hyperthermia is an initial sign of thyroid storm

7. Check BP in upper arm – assesses for Trousseau’s sign (carpopedal spasm is induced by occluding the blood flow to the arm for 3 minutes with a BP cuff)

8. Steam Inhalation to soothe irritated airways9. Observe for signs and symptoms of potential

complications- Hemorrhage- Airway obstruction- Tetany- Recurrent laryngeal nerve damage- Thyroid crisis/storm/thyrotoxicosis- Myxedema (accumulation of mucopolysaccharides

in subcutaneous and other insterstitial tissues secondary to hypothyroidism)

10. Client Teaching Encourage ROM exercises of the neck 3-4 times a day

after discharge Apply cocoa butter lotion over incision site to minimize

scarring Teach about monitoring S/S of THYROID STORM:

a. Causes – stress, infection, unprepared thyroid surgery

b. Manifestations:- Hyperthermia (initial sign!)- ↑ BP, HR and RR with dysrhythmias- Tremors, apprehension, restlessness

- Delirium, psychosis and comac. Management:

- Monitor temp, I/O, neurologic and cardiovascular status q hour

- Provide hypothermic blankets, ice packs and a cool environment to reduce hyperthermia

- Administer hydrocortisone to treat shock or adrenal insufficiency

- Administer O2 to improve tissue oxygenation and to meet the high metabolic demands

- Administer IVF containing dextrose to replace liver glycogen stores that have been decreased

- Administer PTU or methimazole to impede formation of thyroid hormone

- Administer iodine to decrease T4 output from the thyroid gland

- Administer propanolol combined with digitalis to reduce severe cardiac symptoms.

ADDISON’S DISEASE(Adrenocortical Insufficiency)- Results when adrenal cortex function is

inadequate to meet the patient’s need for cortical hormones- Hyposecretion of adrenal cortex hormones

(i.e., sugar, salt, sex)

Causes1. Autoimmune or idiopathic atrophy of the adrenal glands (80%)2. Surgical removal of both adrenal glands3. Infection of the adrenal glands (Tuberculosis and histoplasmosis)4. Inadequate secretion of ACTH from the pituitary gland5. Therapeutic use of corticosteroids

Manifestationsa. Muscle weaknessb. Anorexiac. Gastrointestinal symptomsd. Fatiguee. Emaciationf. Dark pigmentation of the skin, knuckles, knees, elbows and mucous

membranesg. Hypotension h. Hypoglycemia, hyponatremia, hyperkalemiai. Mental status changes – 60-80% of patientsj. Severe, chronic dehydration – severe cases of sodium and potassium

disturbances

Addisonian Crisis- Develops as a result of disease progression

and acute hypertension characterized by cyanosis and the classic signs of circulatory shock

- May be triggered the stress of surgery or dehydration resulting from preparation for diagnostic tests or surgery

- Manifestations:a. Pallorb. Apprehensionc. Rapid and weak pulsed. Rapid respirationse. Low BPf. Headacheg. Nauseah. Abdominal paini. Diarrheaj. Confusion and restlessness

Diagnostics1. ACTH Stimulation Test

- This is the most specific test- Short-acting- Synthetic ACTH is given by IV and blood and

urine cortisol levels are measured and repeated 30-60 minutes after

- Normal values: ↑ blood and urine cortisol levels

- Hypofunction of adrenal cortex: ↓ blood and urine cortisol levels

2. CRH Stimulation Test - Performed when ACTH test is abnormal- Synthetic CRH is injected intravenously and

blood cortisol is measured before and 30, 60, 90, and 120 minutes after the injection

- ↑ ACTH but no cortisol: pituitary defect- ↓ ACTH with deficient cortisol: hypothalamic

defect

Medical and Nursing Interventions1. Replace deficient adrenal cortex hormones

a. Hydrocortisone – synthetic glucocorticoid; taken ONCE or TWICE daily (2/3 [20mg] of dose in the morning, 1/3 [10mg] of dose in the afternoon); don’t give evening doses because this may cause INSOMNIAb. Fludrocortisone – synthetic mineralocorticoid; restoration of normal renin level – best indicator of adequate treatmentc. Addisonian Crisis:

- D5NSS + 100mg Hydrocortisone over 2 hours initially to correct hypoglycemia- NSS to treat dehydration and hyponatremia

- Vasopressors to treat hypotension- Antibiotics to treat infection if it caused the crisis- Oral intake is resumed as soon as tolerated (↓ IV fluids)

2. Diet: High-caloric, high-protein to treat dehydration and high-sodium to replace sodium losses in GI disturbances and very hot weather

3. Monitor BP and I/O

CUSHING’S SYNDROME- Results from excessive adrenocortical

activity- Triggered by excessive administration of

corticosteroids or ACTH or from hyperplasia of the adrenal cortex- ↑ salt, sugar, sex hormones

Manifestations- Alteration of the functions of cortisol:

helps maintain blood pressure and cardiovascular function

helps slow the immune system's inflammatory response

helps balance the effects of insulin in breaking down sugar for energy

helps regulate the metabolism of proteins, carbohydrates, and fats

helps maintain proper arousal and sense of well-being

a. ↑ mineralocorticoids – edema, moon-face, hypertension, heart failureb. ↑ glucocorticoids – truncal obesity, central obesity, buffalo hump,

susceptibility to infection, hyperglycemia or overt diabetesc. ↑ androgens – hirsutism, atrophy of breasts, clitoral enlargement,

deepening of voice, cessation of menses, decreased libido in both men and women

d. muscle wasting and osteoporosis - ↑ protein catabolism

Diagnosticsa. Dexamethasone suppression test

- Widely used screening test- 1 mg dexamethasone is give p.o. at 11 PM and plasma cortisol level is taken 8 AM the next morning- If ↑: Cushing’s Disorder

Medical Managementa. Adrenalectomy

- Treatment of choice in patients with primary adrenal hypertrophy- Adrenal insufficiency appears 12-48 hours post-op: treated with hydrocortisone for several months

- For bilateral adrenalectomy: lifetime replacement of adrenal cortex hormones

b. Transsphenoidal hypophysectomy- Treatment of choice for secondary disease i.e., caused by pituitary tumors instead of tumors of the adrenal cortex- 90% success rate

c. Adrenal enzyme inhibitors- reduce hyperadrenalism if the disease is caused by ACTH oversecretion by a tumor that cannot be eradicated1. Aminogluthethemine - ↓ cholesterol (source of steroids)2. Ketoconazole - ↓ glucocorticoid synthesis (side-effect used as therapeutic effect)3. Mitotane – direct suppression of adrenal cortex4. Metyrapone – blocks cortisol synthesis (similar to mitotane but more on diagnostics than cure)

Nursing Management1. Provide safety – prevent falls, fractures and other injuries to bones and soft tissues2. Diet: High in protein, calcium and vitamin D to minimize muscle wasting and osteoporosis3. Avoid infection – due to ↓ anti-inflammatory effects4. Encourage rest and activity.5. Provide meticulous skin care.6. Provide emotional and psychological support.

DIABETES MELLITUS- Group of metabolic diseases characterized

by elevated levels of glucose in the blood (hyperglycemia) resulting from defects in insulin secretion, insulin action, or both.

- “Starvation in the midst of plenty"

Insulin- Secreted by the beta cells of the Islets of Langerhans in the pancreas- Anabolic, or storage, hormone- Functions:

a. Transports and metabolizes glucose for energyb. Stimulates storage of glucose in the liver and muscle (in the form of

glycogen)c. Signals the liver to stop the release of glucosed. Enhances storage of dietary fat in the adipose tissuee. Accelerates transport of amino acids into cells f. Inhibits the breakdown of stored glucose, protein and fat

- Works together with glucagon to maintain constant level of glucose in the blood

Simple Pathophysiology

Hyperglycemia

Cell hunger Osmotic diuretic effect of excess glucose

Hypothalamus Polyuria

Hunger Intracellular dehydration

Polyphagia Thirst mechanism activated

Polydipsia

Cell looks for other non-CHO sources(Gluconeogenesis)

CHON depletion Fats (CHON breakdown) (Lipolysis)

Weight loss, muscle wasting Fatty AcidsHyperlipidemia

↑ Ketone bodies Atherosclerosis

↓ pHMacroangiopathy,

Microangiopathy, Metabolic acidosis

Neuropathy

Risk Factorsa. Family history of diabetesb. Obesity (≥ 20% over desired body weight) – adipose tissues are

resistant to insulin, therefore glucose uptake by the cells is poorc. Age ≥ 45 yearsd. Previously identified impaired fasting glucose or impaired glucose

tolerancee. History of gestational diabetes or delivery of babies over 9 lbsf. Viral Infection – increased risk to autoimmune disorders

Classification of Diabetes1. Type 1 Diabetes2. Type 2 Diabetes3. Gestational Diabetes4. Diabetes Mellitus associated with other

conditions

Criteria Type 1 Type 2 Gestational DM

DM r/t other conditions

Previous Juvenile Adult-onset Gestational Secondary

Names

diabetes, Juvenile onset, Ketosis-prone

DM Insulin-dependent diabetes

mellitus (IDDM)

diabetes, Ketosis-resistant diabetes, Non-

insulin-dependent diabetes mellitus (NIDDM)

diabetes diabetes

Age at OnsetUsually young;

less than 30 years

Usually over 30 years

During pregnancy,

usually in the 2nd

or 3rd trimester

Any age

CauseBeta cell

desructionInsulin

resistance

Human placental lactogen secretion

Pancreatic diseases, hormonal

abnormalities, medications

Insulin Production

Absent or very little insulin

Decreased insulin or

increased insulin resistance

Inhibited action due to the placental hormone,

human placental lactogen

Age at pregnancy

Ketoacidosis PresentRare, except in

stress or infection

Absent

Depending on the ability of the

pancreas to secrete insulin

Complication Diabetic

ketoacidosis (DKA)

Hyperglycemic, hyperosmolar,

nonketotic syndrome (HHNKS)

Progression to Type 2 DM

Same as with other types

depending on the insulin production

Management Insulin to preserve life

Weight loss, exercise, dietary

modification, oral antidiabetic agents, insulin in some cases

Diet, and if needed, insulin

Depends; oral antidiabetic

agents or insulin

Criteria for the Diagnosis of Diabetes Mellitus (any of these)1. Symptoms of diabetes + random blood sugar ≥ 200 mg/dL

“random” – any time of day without regard to time since last meal “symptoms” – polyuria, polydipsia, polyphagia and unexplained weight loss

2. Fasting blood sugar ≥ 126 mg/dL“fasting” – no caloric intake for at least 8 hours

3. 2-hour postprandial blood sugar ≥ 200 mg/dL uses a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water as in an oral glucose tolerance test

Note: In absence of symptoms, these criteria should be confirmed by repeat testing on a different day.

Impaired fasting glycemia - fasting glucose levels between 100 and 125 mg/dLImpaired glucose tolerance - plasma glucose at or above 140 mg/dL 2 hours after a 75 g oral glucose load; major risk factor for progression to full-blown diabetes mellitus as well as cardiovascular disease.

Other Diagnostic Tests1. Oral Glucose Tolerance Test

- The patient should have fasted for at least 8 hours- Test done in the morning (glucose tolerance is better in the morning)- Given glucose solution P.O. (1.75 g/kg of weight to a maximum of 75 g)- Blood specimen is collected after 30 minutes, 1°, 2° (glucose should return to normal), 3°, 4° or 5° as required

2. Glycosylated Hemoglobin- A form of hemoglobin used primarily to identify the average plasma glucose concentration over prolonged periods of time- Usually done to assess effectiveness of therapy- In the normal 120-day life span of the RBC, excess glucose bind with hemoglobin forming glycated hemoglobin; if ↑, poorly controlled diabetes

3. Urine Exam (Benedict’s Test)- Renal threshold is 180-200 mg/dL- Color changes:

Blue Green –----------- Trace glucoseGreen ------------------- +1Yellow Green --------- +2Yellow Orange ------- +3Orange/Brick Red -- +4

Diabetes Management

Nutrition- Control of total caloric intake to attain or

maintain a reasonable body weight and control of blood glucose levels: most important objective

- Diet is highly individualized and should consider the patient’s food preferences, lifestyle, usual eating times, and ethnic and cultural background

- Ordinary Caloric Requirements/day: 30 cal/kg/day

- Diabetic diet: Carbohydrates 50 – 60%Fats 20 – 30%Protein 10 – 20%

- ↑ Fiber intake: soluble fiber is related to the formation of a gel in the GI tract that slows stomach movement thus decreasing glucose absorption. Insoluble fiber increases stool bulk and preventing constipation.

Exercise- Lowers the blood glucose levels by

increasing muscular uptake of glucose and improving insulin utilization- Don’t exercise until urine tests negative for

ketones and serum glucose is closer to normal! → aggravates hyperglycemia

- Encourage regular daily exercise rather than sporadic exercise

- Usually done 1-2 hours after a meal to cut the need for a pre-exercise snack

- Monitor blood glucose before and after exercise

- Snacks before (fruit exchange) and after exercise in some cases

Medications1. Oral Hypoglycemic Agents

- Effective for patients who have Type 2 diabetes that cannot be treated by diet and exercise alone

a. Sulfonylureas – directly stimulates pancreas to secrete insulin- Take before meals- Avoid alcohol intake when in therapy (produces a disulfiram type of reaction)- e.g. Glipizide

b. Biguanides – facilitates insulin’s action on peripheral receptor sites- Metformin (Glucophage)- Monitor for lactic acidosis and renal dysfunction- Enhanced function when combined with sulfonylureas

c. Alpha-Glucosidase Inhibitors – delays the absorption of glucose in the intestinal system- Acarbose (Precose)- Taken immediately before a meal because it affects food absorption

d. Thiazolinediones – enhances insulin action at the receptor sites without increasing secretion from the pancreas- Can cause resumption of ovulation in perimenopausal anovulatory women making pregnancy a possibility- Rosiglitazone (Avandia)

e. Meglitinides – lowers the blood glucose levels by stimulating insulin release- Taken before each meal

2. Insulina. Short-Acting

- Regular: clear insulin (Humulin R, Semilente)- Onset: 30 minutes - 1 hour- Peak: 2 - 4 hours - Duration: 6 - 8 hours- Hypoglycemia occurs: before lunch (+4 hours) if administered at 7 AM

b. Intermediate-Acting- NPH/Neutral Protamine Hagedorn (Humulin N, Lente)- Onset: 1 – 2 hours- Peak: 6 - 8 hours- Duration: 18 - 24 hours- Hypoglycemia occurs: before supper (+12 hours) if administered at 7 AM

c. Long-Acting- Ultralente- Onset: 3 – 4 hours- Peak: 16 - 20 hours- Duration: 30 – 36 hours- Hypoglycemia occurs: before breakfast (the following day if administered at 7 AM

Nursing Responsibilities in Insulin Therapy:1. Route: Subcutaneous

- Less painful route- In cases of DKA, insulin is given per IV- Do not massage the site of injection

2. Administer at ROOM TEMPERATURE- Prevents the development of cold lipodystrophy

3. Rotate the site of injection- Prevents lipodystrophy which could inhibit insulin absorption- Do not inject into the limb that will be exercised because it will be absorbed faster resulting to hypoglycemia

4. Store vial of insulin in current use at ROOM TEMPERATURE- Ready for injection; unopened vials should be refrigerated- Used vials should not be stored for more than 1 month

5. Gently roll vial in between the palms to redistribute insulin particles- Prevents bubble formation that may make it difficult to aspirate exact amount

6. Observe for side effectsa. Localized

Induration or redness, swelling and tenderness – appears at the injection site 1-2 hours after the insulin administration but disappears with continued use; give antihistamine 1 hour before the injection as prescribed by doc

Lipodystrophy – delays absorption of insulin; don’t administer in these areas, rotate injection sites to prevent

this, injections to the site may be resumed once the hypertrophy disappears

b. SystemicMorning Hyperglycemia:- Dawn Phenomenon: relatively normal blood glucose until 3 AM when the levels begin to rise; due to nocturnal surges of growth hormone that create a greater need for insulin; change time of injection of evening intermediate-acting insulin from dinnertime to bedtime as treatment- Insulin Waning: progressive rise in blood glucose from bedtime to morning; increase evening dose of intermediate or long acting insulin as treatment- Somogyi Effect: normal or elevated blood glucose at bedtime, a decrease at 2-3 AM to hypoglycemic levels, and a subsequent increase caused by production of counterregulatory hormones; decrease evening dose of intermediate acting insulin or increase bedtime snack

Hypoglycemia:Causes: skipping of meals, overexercise, overdosage of insulinManifestations: Cold, clammy skin, diaphoresis, tremors and tachycardia, irritability, dizziness, blurred vision, altered LOC (“Cold and clammy needs candy”)Interventions: - Allow patient to eat- Give simple sugars P.O.:

3 –4 commercially prepared glucose tablets4 – 6 oz of fruit juice or regular soda6 – 10 Life Savers or other hard candies2 – 3 teaspoons of sugar or honey

- If unconscious: D50W 25 - 50 mL IV- Monitor blood sugar

HyperglycemiaType 1: Diabetic Ketoacidosis

Causes: absence or markedly inadequate amount of insulin causing an increased conversion of fatty acids into ketone bodiesTriggers: decreased or missed dose of insulin, illness or infection, undiagnosed and untreated diabetesOnset: Rapid (<24 hours)Blood Glucose Levels: >250 mg/dLMortality: <5%Manifestations: Hyperglycemia, dehydration and electrolyte loss and acidosisManagement: a. Rehydration

- NSS IV fast drip (0.5-1 L/hour for 2-3 hours)

- D5W when blood glucose reaches 300 mg/dL- Monitor signs of fluid overload- Plasma expanders to correct severe

hypotension that do not respond to IV therapy

b. Restoring Electrolytes- Potassium replacement begins once

potassium levels drop to normal following rehydration and insulin treatment. Withhold when the patient is not urinating.

c. Reversing Acidosis- NSS + insulin IV (drip)- Must be continued even if blood glucose levels

are dropping to prevent reaccumulation of ketone bodies

Type 2: Hyperglycemic Hyperosmolar Nonketotic Syndrome

Causes: caused by lack effective insulinTrigger: Physiologic stress (infection, surgery, CVA, MI)Onset: Slower (over several days)Blood Glucose Levels: Usually >600 mg/dLMortality Rate: 10-40%Manifestations: hypotension, profound dehydration, tachycardia, variable neurologic signsManagement: a. Fluid and electrolyte replacement

- Plain NSS or 0.45 NS depending on the sodium level

- Insulin at a continuous low rate to treat hyperglycemia

b. Follow up laboratory resultsc. Close monitoring of vital signs

EducationInstruct about FOOT CARE:a. Take care of your diabetes.b. Inspect your feet every day (look for wounds and feel for changes in

temperature)c. Wash your feet every day with warm water. Do not soak. Do not feel

temperature with your feet.d. Pat dry your feet – do not rub.e. Keep the skin soft and smooth by applying lotion over tops and bottoms of

feet but not between toes.f. Smooth corns and calluses gently.g. Trim your toenails each week or when needed. Straight across and file the

edges.h. Wear properly fitting and comfortable shoes and socks at all timesi. Protect your feet from hot and cold.j. Keep the blood flowing to your feet. Put your feet up when sitting. Do not

cross your legs for long periods of time. Do not smoke.

k. Check with your doctor if you found out foot problems. Do not self medicate!