THE ENDOCRINE SYSTEM

Endocrine System Consists primarily of the pituitary, thyroid, parathyroid, adrenals, the islets of Langerhans in the pancreas and the gonads. Functions Participates in the regulation of digestion, use and storage of nutrients. Growth and development Electrolyte and water metabolism Reproductive functions Hormones Chemical substances that act as messengers to specific cells and organs, stimulating and inhibiting various processes. 2 major categories: Local – specific effect on the area of secretion. General – transported in the blood to distant sites where they exert their effect.Hormone Regulation 1. Negative feedback - major means of regulating hormone levels. Decreased concentration of a circulating hormone triggers production of a stimulating hormone from the pituitary gland. This in turn stimulates its target organs to produce hormones. Increased concentration of a hormone inhibits the production of the stimulating hormone, resulting to decreased secretion of the target organ. 2. Controlled by changing blood levels of specific substances like calcium and glucose. 3. Certain hormones follow rhythmic patterns of secretion e.g. cortisol and female reproductive hormones. 4. Autonomic and CNS control Assessment Subjective: Determining onset, frequency, duration, alleviating or aggravating factors, chronology of events, associated symptoms, quantity and intensity of symptoms. Health History Presenting Symptoms: Change in appearance Change in energy levels Temperature intolerance Development of abnormal secondary characteristics. Change in emotional states Change in bowel and urinary habits.

Potential Symptoms: General: easy fatigability, lethargy, insomnia, weight loss or weight gain Skin, hair and nails : dry scaly skin, patches of increased or decreased pigmentation, hair loss, brittle nails. Head and face : puffy face and eyelids, red eyes, voice changes, enlarging neck Potential symptoms:

Cardiovascular: palpitations Gastrointestinal: constipation, polyphagia, polydipsia, dysphagia Neurologic : tremors, memory loss Genitourinary: amenorrhea, menorrhagia, polyuria Musculoskeletal: muscle aching and weakness Objective general assessment: Note height, weight, body stature and body proportions Observe distribution of muscle mass and fat distribution. Assess integrity of skin. Note lesions, warmth, moisture and pigmentation. Inspect hair growth and distribution. Inspect eyes for bulging. Observe enlargement of neck and quality of voice. Observe development of secondary sex characteristics.

HYPOPITUITARISM Underactivity of the anterior pituitary gland. Manifested by partial or complete deficiency of hormone production. Cause Neoplasms Trauma Surgical removal Irradiation of the gland Congenital anomalies Postpartum hemorrhage Inflammation or infection Assessment Headache tumor expansion Visual field deficits and pressure on the Cranial nerve palsy optic chiasma. Menstrual dysfunction Growth retardation - Dwarfism Diagnostic TestsRadiologic exam Thyroid function tests Neuroopthalmologic evaluation Visual acuity Extraocular muscle function Diagnosis is often delayed since ¾ of the gland has to be destroyed before signs and symptoms occur. Therapeutic Management Surgical removal X ray irradiation Hormonal replacement Corticosteroids 15-60mg Levothyroxine Gonadotropins Pituitary Apoplexy Acute pituitary failure caused by tumor enlargement and hemorrhage Temporary stabilization with high dose corticosteroids. Nursing Management

Assessment should be ongoing. Provide care for the client undergoing irradiation. Provide client teaching and planning for discharge. For corticosteroid therapy: Administer with food or milk. Report gastric problems Give at 9am. ( Corticosteroids suppresses adrenal function least when givn early morning. ) Infection control.

HYPERPITUITARISM Hyperfunction of the anterior pituitary gland resulting in oversecretion of one or more of the anterior pituitary hormone. Acromegaly – hypersecretion of the growth hormone occurs after puberty resulting in bone and connective tissue continuing to grow which results to enlarged face, hand and feet. Gigantism – hypersecretion of the growth hormone occurs prior to puberty resulting in the person becoming excessively tall. Causes: Benign pituitary tumor Macroadenoma – grows rapidly but contains less GH Microadenoma – grows slower but have more GH Systemic pathologic processes and disease follows: Kyphosis Premature arthritis of the weight bearing joints. Peripheral neuropathy due to nerve entrapment. assessment Coarsened facial features Prognathasia ( forward projection of the jaws) Macroglossia ( enlargement of the tongue) Prominence of the forehead and orbital ridges Joint pains Spadelike hands Paresthesias Diagnostic tests Radiographic tests CT scan and MRI Serum GH level, serum somatomedin level increased Goal of therapeutic management Returning GH levels to normal Reversing associated physiologic and metabolic abnormalities Avoid systemic complications and tumor enlargement Preventing recurrence SURGERY and RADIOTHERAPY

CARE OF THE PATIENT UNDERGOING TRANSSPHENOIDAL HYPOPHYSECTOMY 1. Preoperative Management Sinus infection is assessed and treated, if necessary. Hydrocortisone (Cortef) may be given preoperatively because the source of ACTH is being removed. The patient is prepared physically and emotionally for surgery. Deep-breathing exercises. Avoid coughing and sneezing postoperatively to prevent CSF leak. Protecting Against Complications Monitor vital signs, visual acuity, and neurologic status frequently for signs of increasing intracranial pressure. Monitor fluid intake and output, and report any increase in output and decrease in specific gravity, which may indicate DI. Report persistent clear fluid from nose and increasing headache; could signal CSF leak. Teach patient signs of complications and to report them immediately and to follow-up as scheduled. Assess level of pain and administer analgesic or supervise patient-controlled analgesia. Preventing Infection Observe for signs of infection. Check incision within inner aspect of upper lip for drainage or bleeding. Note frequency of nasal dressing changes and character of drainage. Prepare patient for packing removal one to several days postoperatively. Encourage the use of a humidifier to prevent drying from mouth breathing. Nursing care Monitor cardiovascular status. Provide support in OR/Radiotherapy. Psychological support and accepting attitude in body image disturbance.

DIABETES INSIPIDUS a disorder of water metabolism caused by deficiency of ADH, also called vasopressin, secreted by the posterior pituitary or by inability of the kidneys to respond to ADH Causes: Primary: idiopathic. Secondary: head trauma, neurosurgery, tumors (intracranial or metastatic), vascular disease (aneurysms, infarct), infection (meningitis, encephalitis). Nephrogenic DI: long-standing renal disease, hypokalemia, some medications AssessmentMarked polyuria - daily output of 5 to 20 L of dilute urine; appearance of urine like that of water Polydipsia (intense thirst) - drinks 4 to 40 L of fluid daily; has craving for cold water.

High serum osmolality (above 295 mOsm) and high serum sodium level (greater than 145 mEq/L). Diagnostic Tests Urine specific gravity less than 1.004 ADH count decreased or absent Water Deprivation Test Therapeutic Management Administration of ADH or its derivative. Desmopressin acetate (DDAVP) - vasopressin derivative administered into the nose through a soft, flexible nasal tube or by nasal spray. Duration of action 12 to 24 hours. For patients who have some residual hypothalamic ADH (determined by low levels of circulating ADH). Chlorpropamide (Diabinese) - potentiates action of vasopressin on renal-concentrating mechanism. Clofibrate (Atromid-S) - probably acts by augmenting ADH secretion from posterior pituitary. Carbamazepine (Tegretol) - potentiates action of endogenous vasopressin. Maintaining Adequate Fluid Volume Measure fluid intake and output accurately. Obtain daily weights. Monitor hemodynamic status, as indicated, via frequent BP, heart rate, central venous pressure, and other measurements. Provide patient with ample water to drink and administer I.V. fluids as indicated. Monitor results of serum and urine osmolality and serum sodium tests. Administer or teach self-administration of medication as prescribed and document patient response Patient Education and Health Maintenance Inform the patient that metabolic status must be monitored on a long-term basis because the severity of DI changes from time to time. Advise patient to avoid limiting fluids to decrease urine output; thirst is a protective function. Advise patient to wear a MedicAlert bracelet stating that the wearer has DI. Teach patient to be alert for signs of dehydration decreased weight, decreased urine output, increased thirst, dry skin and mucous membranes; and overhydration increased weight and edema and report these to the health care provider. Tell the patient to consider eliminating coffee and tea from die tmay have an exaggerated diuretic effect. Give written instruction on vasopressin administration. Have the patient demonstrate intranasal and injection technique.

HYPERPARATHYROIDISM Most common among women older than age 50. Primary hyperparathyroidism. Single parathyroid adenoma is the most common cause (approximately 80% of cases). Secondary hyperparathyroidism. Primarily the result of renal failure. Assessment Decalcification of bones. Skeletal pain, backache, pain on weight-bearing, pathologic fractures, deformities, formation of bony cysts. Formation of bone tumors overgrowth of osteoclasts. Formation of calcium-containing kidney stones. Depression of neuromuscular function. The patient may trip, drop objects, show general fatigue, lose memory for recent events, experience emotional instability, have changes in level of consciousness, with stupor and coma. Cardiac arrhythmias, hypertension, cardiac standstill. Diagnostic Tests Serum PTH level is increased. Serum calcium is elevated Decrease in serum phosphorus level. Xray reveals skeletal changes. Therapeutic ManagementHydration (I.V. saline) and diuretics-furosemide (Lasix) and ethacrynic acid (Edecrin) to increase urinary excretion of calcium in patients not in renal failure. Oral phosphate may be used as an antihypercalcemic agent. Calcitonin (Cibacalcin), or etidronate disodium (Didronel) are effective in treating hypercalcemia by inhibiting bone resorption. Removal of underlying cause. •Dietary calcium is restricted, and all drugs that might cause hypercalcemia (thiazides, vitamin D) are discontinued. •Dialysis may be necessary in patients with resistant hypercalcemia or those with renal failure. •Digoxin is reduced because patient with hypercalcemia is more sensitive to toxic effects of this drug. •Monitoring of daily serum calcium, blood urea nitrogen (BUN), potassium, and magnesium levels.

Achieving Fluid and Electrolyte Balance Monitor fluid intake and output. Provide adequate hydration administer water, glucose, and electrolytes orally or I.V. as prescribed.

Prevent or promptly treat dehydration by reporting vomiting or other sources of fluid loss promptly. Help patient understand why and how to avoid dietary sources of calcium dairy products, broccoli, calcium-containing antacids. Promoting Urinary Elimination Strain all urine to observe for stones. Increase fluid intake to 3,000 mL/day to maintain hydration and prevent precipitation of calcium and formation of stones. Instruct the patient about dietary recommendations for restriction of calcium. Observe for signs of urinary tract infection (UTI), hematuria, and renal colic. Assess renal function through serum creatinine and BUN levels. Increasing Physical Mobility Assist the patient in hygiene and activities if bone pain is severe or if the patient experiences musculoskeletal weakness. Protect the pent from falls or injury. Turn the patient cautiously and handle extremities gently to avoid fractures. Administer analgesia as prescribed. Assess level of pain and the patient's response to analgesia. Encourage the patient to participate in mild exercise gradually as symptoms subside. Instruct and demonstrate correct body mechanics to reduce strain, backache, and injury.

HYPOPARATHYROIDISM The most common cause is accidental removal or destruction of parathyroid tissue or its blood supply during thyroidectomy or radical neck dissection for malignancy. Decrease in gland function (idiopathic hypoparathyroidism); may be autoimmune or familial in origin. Malignancy or metastasis from a cancer to the parathyroid glands. Assessment Tetany - general muscular hypertonia; attempts at voluntary movement result in tremors and spasmodic or uncoordinated movements; fingers assume classic tetanic position. Chvostek's sign Trousseau's sign Laryngeal spasm. Severe anxiety and apprehension. Renal colic is usually present if the patient has history of stones; preexisting stones loosen and migrate into the ureter. Diagnostic TestsDecreased PTH level Increased phosphorus level Decreased calcium level

Therapeutic Management A syringe and an ampule of a calcium solution (calcium chloride, calcium gluceptate, calcium gluconate) are to be kept at the bedside at all times. Most rapidly effective calcium solution is ionized calcium chloride (10%). For rapid use to relieve severe tetany, infusion carried out every 10 minutes. All I.V. calcium preparations are administered slowly. It is highly irritating, stings, and causes thrombosis; patient experiences unpleasant burning flush of skin and tongue. Typical doses are as follows: Calcium chloride 500 mg to 1 g (5 to 10 mL) as indicated by serum calcium; administer at rate of less than 1 mL/minute of 10% solution. Calcium gluconate 500 mg to 2 g (10 to 20 mL) at a rate of less than 0.5 mL/minute of a 10% solution. Calcium gluceptate 1 to 2 g (5 to 10 mL) at a rate of less than 1 mL/minute. A slow drip of I.V. saline containing calcium gluconate is given until control of tetany is ensured; then I.M. or oral administration of calcium is prescribed. Later, vitamin D is added to calcium intake increases absorption of calcium and also induces a high level of calcium in the bloodstream. Thiazide diuretics may also be added because of their calcium-retaining effect on the kidney; doses of calcium and vitamin D may be lowered. Maintaining Calcium Levels Assess neuromuscular status frequently in patients with hypoparathyroidism and in those at risk for hypocalcemia (patients in the immediate postoperative period after thyroidectomy, parathyroidectomy, radical neck dissection). Check for Trousseau's and Chvostek's signs and notify health care provider if tests results are positive. Assess respiratory status frequently in acute hypocalcemia and postoperatively. Monitor serum calcium and phosphorus levels. Promote high-calcium diet if prescribed—dairy products, green, leafy vegetables. Instruct the patient about signs and symptoms of hypo- and hypercalcemia that should be reported. Use caution in administering other drugs to the patient with hypocalcemia. The hypocalcemic patient is sensitive to digoxin (Lanoxin); as hypocalcemia is reversed, the patient may rapidly develop digitalis toxicity.

Cimetidine (Tagamet) interferes with normal parathyroid function, especially with renal failure, which increases the risk of hypocalcemia. DIABETES MELLITUS DM is a metabolic disorder affecting a variety of physiologic systems, the most critical of which involves glucose metabolism. Results from a a deficiency of insulin. Abnormality causes:Hyperglycemia Hyperlipidemia hyperaminoacidemia Risk factors: Family history of diabetes Obesity Race/Ethnicity Age History of gestational diabetes Major classification:1. Type 1 Diabetes Mellitus ( Insulin Dependent/Juvenile DM) Little or no endogenous insulin, requiring injections of insulin to control diabetes and prevent ketoacidosis. Five to 10% of all diabetic patients have type Etiology: autoimmunity, viral, and certain histocompatibility antigens as well as a genetic component. Usual presentation is rapid with classic symptoms of polydipsia, polyphagia, polyuria, and weight loss. Most commonly seen in patients under age 30 but can be seen in older adults Type 2 Diabetes Mellitus ( Non insulin Dependent/Adult onset DM ) Caused by a combination of insulin resistance and relative insulin deficiency some individuals have predominantly insulin resistance, whereas others have predominantly deficient insulin secretion, with little insulin resistance. Approximately 90% of diabetic patients have type 2. Etiology: strong hereditary component, commonly associated with obesity. Usual presentation is slow and typically insidious with symptoms of fatigue, weight gain, poor wound healing, and recurrent infection. Found primarily in adults over age 30; however, may be seen in younger adults and adolescents who are overweight. Gestational Diabetes Mellitus Gestational diabetes mellitus (GDM) is defined as carbohydrate intolerance occurring during pregnancy. Occurs in approximately 4% of pregnancies and usually disappears after delivery. Women with GDM are at higher risk for diabetes at a later date.

GDM is associated with increased risk of fetal morbidity. Screening for GDM for all pregnant women other than those at lowest risk (under age 25, of normal body weight, have no family history of diabetes, are not a member of an ethnic group with high prevalence of diabetes) should occur between the 24th and 28th weeks of gestation. Diabetes Associated with Other Conditions Certain drugs can decrease insulin activity resulting in hyperglycemia corticosteroids, thiazide diuretics, estrogen, phenytoin. Disease states affecting the pancreas or insulin receptors pancreatitis, cancer of the pancreas, Cushing's disease or syndrome, acromegaly, pheochromocytoma, muscular dystrophy, Huntington's chorea. Pathophysiology Lack of insulin causes: Lowered utilization of blood glucose by body cells resulting in increased serum glucose levels. Mobilization of fatty acids from fat stores resulting in abnormal fat metabolism Decreased protein disposition in body tissues due to lack of protein anabolism which insuin promotes under normal circumstances. Assessment Weight loss, fatigue Polyuria, polydipsia, polyphagia Blurred vision Paresthesias Poor wound healing Recurrent infections, particularly of the skin Diagnostic TestsBlood Glucose For fasting glucose, make sure that patient has maintained 8-hour fast overnight; sips of water are allowed. Advise patient to refrain from smoking before the glucose sampling because this affects the test results. For postprandial test, advise patient that no food should be eaten during the 2-hour interval. For random blood glucose, note the time and content of the last meal. Interpret blood values as diagnostic for diabetes mellitus as follows: FBS greater than or equal to 126 mg/dL on two occasions Random blood sugar greater than or equal to 200 mg/dL and presence of classic symptoms of diabetes (polyuria, polydipsia, polyphagia, and weight loss) Fasting blood glucose result of greater than or equal to 100 mg/dL demands close follow-up and repeat monitoring. Oral Glucose Tolerance Test The oral glucose tolerance test (OGTT) evaluates insulin response to glucose loading. FBS is obtained before the

ingestion of a 50- to 200-g glucose load (usual amount is 75 g), and blood samples are drawn at ½, 1, 2, and 3 hours (may be 4- or 5-hour sampling). Advise patient that for accuracy in results, certain instructions must be followed: Usual diet and exercise pattern must be followed for 3 days before OGTT. During OGTT, the patient must refrain from smoking and remain seated. Oral contraceptives, salicylates, diuretics, phenytoin, and nicotinic acid can impair results and may be withheld before testing based on the advice of the health care provider. Diagnostic for diabetes mellitus if 2-hour value is 200 mg/dL or greater. Glycated Hemoglobin (Glycohemoglobin, HbA1c) Measures glycemic control over a 60- to 120-day period by measuring the irreversible reaction of glucose to hemoglobin through freely permeable erythrocytes during their 120-day lifecycle. No prior preparation, such as fasting or withholding insulin, is necessary. Test results can be affected by red blood cell disorders (eg, thalassemia, sickle cell anemia), room temperature, ionic charges, and ambient blood glucose values. Many methods exist for performing the test, making it necessary to consult the laboratory for normal values. Therapeutic Management Goal: Complete normalization of glycemia. Treatment includes: Alleviate symptoms. Avoidance of acute complications. Protection from untoward effects of the regimenDawn Phenomenon – Relatively normal blood glucose until about 3am when the level begins to rise. Somogyi Effect – Nocturnal hypoglycemia followed by a rebound hyperglycemia. Treatment Modality 1.Diet Dietary control with caloric restriction of carbohydrates and saturated fats to maintain ideal body weight. The goal of meal planning is to control blood glucose and lipid levels Meal Planning Guidelines Each meal should consist of a balance of carbohydrates, proteins, and fats. Consistency in timing of meals and amounts of food eaten on a day-to-day basis help regulate blood glucose levels. Increase the intake of soluble and insoluble fiber. Avoid salt whenever possible Prepare foods to retain vitamins and minerals and reduce fats.

Distribute snacks in the meal plan depending on insulin/medication regimens, physical activity, and lifestyle Use alcohol only in moderation Use alternative nonnutritive, noncaloric sweeteners in moderation Exercise Regularly scheduled, moderate exercise performed for at least 30 minutes most days of the week promotes the utilization of carbohydrates, assists with weight control, enhances the action of insulin, and improves cardiovascular fitness. Oral Hypoglycemics 1.Sulfonylureas – glipizide, glimepiride 2.Biguanides – metformin ( Glucophage ) 3.Glucosidase inhibitors – acarbose, miglitol 4.Thiazolidinediones – rosigitazone, pioglitazone

INSULINONSE

TPEAK

DURATION

Immediate-acting(lispro, aspart)

0.25 hour

0.5-1 hour

5 hours

Short-acting(regular,

semilente)

0.5-1 hour

2-4 hours

5-7 hours

Intermediate-acting(NPH, lente)

1-3 hours

6-12 hours

18-24 hours

DANGER!!! Insulin Shock Abnormally low blood sugar usually below 50mg/dL Caused by insulin overdosage or rapid onset. Assessment: headache, dizziness, slurred speech Nursing care: Administer oral sugar D5050Nursing Care Observe for signs of hypo/hyperglycemia by monitoring. Provide meticulous skin care. Provide special diet as ordered. Client should be able to plan meals usng exchange list. Emphasize importance of regularity of meals; never skip meals. Maintain I & O. Observe insulin therapy guidelines: Use insulin at room temperature. Gently roll between palms Observe sterile technique Aspirate clear first befre cloudy. Systematically rotate sites to prevent lipodystrohy. Foot care: Wash feet with mild soap and water.

Apply lanolin to prevent cracking. Cut toenails straight across. Avoid constricting garments. Wear clean, absorbent socks. Use proper fitting shoes. Never go barefoot. Massage the feet with an absorbable agent. Discuss with the patient the perceived effect of diabetes on lifestyle, finances, family life, occupation. Encourage patient and family participation in diabetes self-care regimen to foster confidence.

COMPLICATIONS OF DIABETES MELLITUS DIABETIC KETOACIDOSIS DKA is an acute complication of diabetes mellitus (usually type 1 diabetes) characterized by hyperglycemia, ketonuria, acidosis, and dehydration. Complication in Type 1 DM Clinical Manifestations Early Polydipsia, polyuria Fatigue, malaise, drowsiness Anorexia, nausea, vomiting Abdominal pains, muscle cramps Later Kussmaul respiration (deep respirations) Fruity, sweet breath Hypotension, weak pulse Stupor and coma Restoring Fluid and Electrolyte Balance Assess BP and heart rate frequently, depending on patient's condition; assess skin turgor and temperature. Monitor intake and output every hour. Replace fluids as ordered through peripheral I.V. line. Monitor urine specific gravity to assess fluid changes. Monitor blood glucose frequently. Assess for symptoms of hypokalemia—fatigue, anorexia, nausea, vomiting, muscle weakness, decreased bowel sounds, paresthesia, arrhythmias, flat T waves, ST-segment depression. •Administer replacement electrolytes and insulin as ordered. Flush the entire I.V. infusion set with solution containing insulin and discard the first 50 mL because plastic bags and tubing may absorb some insulin and the initial solution may contain decreased concentration of insulin. •Monitor serum glucose, bicarbonate, and pH levels periodically. •Provide reassurance about improvement of condition and that correction of fluid imbalance will help reduce discomfort.

HYPEROSMOLAR HYPERGLYCEMIC NONKETOTIC SYNDROME

HHNS is an acute complication of diabetes mellitus (particularly type 2 diabetes) characterized by hyperglycemia, dehydration, and hyperosmolarity, but little or no ketosis. Complication in Type 2 DM. Clinical Manifestation Early Polyuria, dehydration Fatigue, malaise Nausea, vomiting Later Hypothermia Seizures, stupor, coma Muscle weakness Nursing Care Admitted to intensive care unit since this is a life-threatening condition. Correct fluid and electrolyte imbalances giving isotonic and colloid solutions and correct potassium deficits. Lower glucose with regular insulin.