THE ENDOCRINE SYSTEM

Prepared by Crisanto Christopher B. Sanares

I.

Hormones HORMONES STEROIDEx. Hydrocortisone / PEPTIDEEx.PROTEIN HORMONES Insulin MINE HORMONES A Ex. Epinephrine

HYROID STIMULATING HORMONE (TSH) Aka THYROTROPIN Produced by THYROTROPES or thyrotropic cells of the APG Hyposecretion: SECONDARY HYPOTHYRODISM Hypersecretion: SECONDARY HYPERTHYROIDISM

II.

Endocrine Glands A. Major Endocrine Glands 1. Pituitary gland 2. Thyroid gland 3. Parathyroid glands 4. Pancreas 5. Adrenal glands 6. Ovaries Estrogen & Progesterone 7. Testes - Testosterone 8. Hypothalamus GHRH, GHIH, TRH, PIH, CRH, GnRH, MIH, Oxytocin, ADH B. Minor Endocrine Glands 1. Thymus - Thymosin 2. Pineal gland - Melatonin C. Other tissues 1. Placenta HPL, HCG 2. GIT Gastrin, Secretin, Cholecystokinin 3. Kidneys Erythropoietin

P ROLACTIN (PRL) Aka MAMMOTROPIN

Produced by MAMMOTROPES or mammotropic cells of the APG Hyposecretion: POOR MILK SECRETION Hypersecretion: GALACTORRHEA, IMPOTENCE (males), AMENORRHEA (females)

ADRENOCORTICOTROPIC HORMONE (ACTH) Aka CORTICOTROPIN

Produced by CORTICOTROPES or corticotropic cells of the APG Hyposecretion: SECONDARY ADDISONS DISEASE Hypersecretion: SECONDARY CUSHINGS DISEASE

L UTEINIZING HORMONE (LH) & F OLLICLE-STIMULATING HORMONE (FSH)

Aka GONADOTROPINS Produced by GONADOTROPES or gonadotropic cells of the APG Hyposecretion: HYPOGONADISM, SEXUAL MATURATION INHIBITION Hypersecretion: HYPERGONADISM, PRECOCIOUS PUBERTY

III. Diagnostic Test Groups A. Blood Tests 1. determines hormone blood levels 2. Detects antibodies 3. Assesses effect of hormone on other substances (e.g., insulin on glucose) Ex. Radioimmunoassays B. Urine Tests measure amount of hormone or end products of hormones excreted by the kidneys Ex. Vannillylmandelic acid test for pheochromocytoma C. Stimulation or Suppression tests 1. Stimulation tests administration of stimulating hormones (+) response = problem in hypothalamus or pituitary gland (-) response = problem in endocrine gland itself 2. Suppression tests used to determine whether negative feedback mechanisms that normally control secretion of hormones from hypothalamus or pituitary gland are intact IV. PITUITARY GLAND aka HYPOPHYSIS; located at the sella turcica at the base of the brain, overlying the sphenoid bone; located behind the optic chiasma and optic nerves. A. ANTERIOR PITUITARY GLAND (APG) aka ADENOHYPOPHYSIS Produces its own hormones Hormones of APG are regulated by RELEASING AND INHIBITING HORMONES/FACTORS from the HYPOTHALAMUS Made up of 5 CELLS, each cell producing a distinct hormone Collectively, hormones of the APG go with the mnemonic GTPALFM for easy memorization

MELANOCYTE-STIMULATING HORMONE (MSH) of the Believed to be secreted by the Intermediate lobe

APG Has a stimulating effect on the Adrenal Cortex Affects pigmentation Hyposecretion: ALBINISM Hypersecretion: ETERNAL TAN

B.

POSTERIOR PITUITARY GLAND (PPG) aka NEUROHYPOPHYSIS Does not produce its own hormones Hormones of PPG are produced by the Hypothalamus PPG stores and releases these 2 hormones

OXYTOCIN for uterine contraction and milk Necessary

ejection (milk let-down reflex)

ANTIDIURETIC HORMONE (ADH) Aka VASOPRESSIN

Causes water reabsorption in the kidneys Hyposecretion: DIABETES INSIPIDUS (DI) Hypersecretion: SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE (SIADH) C. ENDOCRINE PROBLEMS OF THE PITUITARY GLAND 1. HYPERSECRETION / OVERSECRETION: HYPERPITUITARISM a. Commonly involves ACTH and/or GH b. CUSHINGS SYNDROME and/or ACROMEGALY / GIANTISM

ROWTH HORMONE (GH) Aka SOMATOTROPIN Produced by SOMATOTROPES or somatotropic cells of the APG Hyposecretion: DWARFISM Hypersecretion: GIGANTISM or ACROMEGALY

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HYPOSECRETION / UNDERSECRETION: HYPOPITUITARISM a. Commonly involves all APG hormones b. A rare condition would include all pituitary hormones, a condition known as PANHYPOPITUITARISM or SIMMONDS DISEASE

D. COMMON ENDOCRINE DISORDERS OF THE PITUITARY GLAND 1. ACROMEGALY a. Hypersecretion of GH after epiphyseal plate closure at puberty b. Commonly caused by a GH producing pituitary adenoma (tumor) c. Other causes include non-pituitary tumors in the pancreas, adrenal glands, and lungs by either producing GH or more frequently producing GHRH d. Assessment: Enlargement of the hands, feet, nose, lips and ears, and a general thickening of the skin Soft tissue swelling of internal organs, notably the heart with attendant weakening of its muscularity, and the kidneys, also the vocal cords resulting in a characteristic thick, deep voice and slowing of speech Generalized expansion of the skull at the fontanelle Pronounced brow protrusion, often with ocular distension Pronounced lower jaw protrusion with attendant macroglossia (enlargement of the tongue) and teeth gapping Hypertrichosis, hyperpigmentation, and hyperhidrosis may occur e. Complications: Severe headache Arthritis and carpal tunnel syndrome Enlarged heart (cardiomegaly) Hypertension Diabetes mellitus Heart failure Kidney failure Compression of the optic chiasm leading to loss of vision in the outer visual fields (typically bitemporal hemianopia) Increased palmar sweating and sebum production over the face (seborrhea) are clinical indicators of active growth hormone (GH) producing pituitary tumors. f. Management: The goals of treatment are: o to reduce GH production to normal levels o to relieve the pressure that the growing pituitary tumor exerts on the surrounding brain areas o to preserve normal pituitary function o to reverse or ameliorate the symptoms of acromegaly Surgical removal of the tumor through HYPOPHYSECTOMY o Aka pituitary adenectomy o Done either via craniotomy or transsphenoidal approach (latter approach is preferred because it is associated with fewer complications) o Complications for craniotomy Inc. ICP, bleeding, meningitis, hypopituitarism o Complications for transsphenoidal surgery CSF leak, infection, hypopituitarism

2.

Postop interventions: Monitor V/S, neuro status, LOC, inc. ICP, bleeding, CSF leak (postnasal drip or nasal drainage), electrolytes for temporary DI or SIADH resulting from ADH disturbances, I & O Elevate the head of bed Instruct the client to avoid sneezing, coughing, and blowing the nose Avoid water intoxication Administer glucocorticoids and other hormone replacements as prescribed Administer antibiotics, analgesics, and antipyretics as prescribed Instruct the client in the administration of prescribed medications, which may include vasopressin (synthetic ADH), levothyroxine (Synthroid), gonadotropic hormones, growth hormone, and glucocorticoids if the entire gland has been removed Drug therapy o Somatostatin analogues given by IM or subcutaneous injections; stops GH production lanreotide (Somatuline) octreotide (Sandostatin) inhibits gastrointestinal and pancreatic function loose stools, nausea, gas, gallstone formation which is usually asymptomatic, DM rarely can be used as an antidiarrheal due to its inhibiting effect of GI function by increasing absorption of fluid and electrolytes in the GIT o bromocriptine (Parlodel) in tablet Side-effects: gastrointestinal upset, nausea, vomiting, light-headedness when standing, and nasal congestion Start with a very low dose at bedtime Taken with food Gradually increase dose to the therapeutic dose o Growth hormone receptor antagonist pegvisomant (Somavert) injected subcutaneously daily or can be injected weekly in combination with somatostatin analogues Radiation therapy o

DIABETES INSIPIDUS (DI) a. Hyposecretion of ADH caused by strokes or trauma, or may be idiopathic b. Assessment: Polyuria of 4 to 24 L/day Urine contains NO albumin and/or glucose Inability to concentrate urine Urine osmolality decreases Urine specific gravity decreases (1.001 to 1.005) Polydipsia, patient craves 2-20 liters/day of cold water Dehydration dec. skin turgor, dry mucous membranes Weight loss Hypernatremia

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d.

Serum osmolality increases Fatigue, muscle pain and weakness Headache Postural hypotension that may progress to vascular collapse without rehydration Tachycardia Diagnosis: Fluid Deprivation Test o Withhold fluids for 8-12 H or until 3% 5% of body weight is lost o Patient is weighed frequently during the test o Plasma and urine osmolality are measured at the beginning and at the end of the test o STOP IFTACHYCARDIA, EXCESSIVE WEIGHT LOSS, or HYPOTENSION develops Plasma level of ADH Plasma and urine osmolality o Normal plasma osmolality = 270-300 mOsm/kg water o Normal urine osmolality = 250-900 mOsm/kg water Management: Monitor V/S, neuro, CV status Provide a safe environment, particularly for the client with postural hypotension Replace ADH o DESMOPRESSIN (DDAVP) Used for chronic or severe DI Synthetic vasopressin without the vascular effects of ADH Intranasal (SPRAYED) through flexible calibrated plastic tube Administered OD/BID or every 12 to 24 H o VASOPRESSIN TANNATE IN OIL (Pitressin) Used for chronic or severe DI IM ADH Every 24 to 96 H in the EVENING for maximum results during sleep Vial WARMED or SHAKEN VIGOROUSLY before administration Rotate sites to prevent lipodystrophy Side-effect: Abdominal cramps Caution in patients with CAD; causes vasoconstriction o CLOFIBRATE, CHLORPROPAMIDE potentiate action of vasopressin; used for mild DI Ensure adequate fluid replacement Measure intake and output, weight, serum osmolality, urine specific gravity Identify and correct underlying intracranial pathology Instruct the client to wear a Medic-Alert bracelet.

c.

d.

Hypertension Altered level of consciousness, cerebral edema Tachycardia Anorexia, nausea, vomiting Diagnosis: Blood tests: inc. ADH, dec. serum osmolality, dec. Na (<135 mEq/L) Urinalysis: Inc. urine osmolality, inc. Na Management: Correct underlying cause, if possible Monitor V/S, neuro, CV status Provide safe environment, particularly for the client with LOC changes Restrict fluid intake (500 to 1000 mL/day) If fluid restriction is ineffective, give DEMECLOCYCLINE (DECLOMYCIN) to block the renal response to ADH and produce water dieresis Furosemide (Lasix) with NSS or hypertonic saline to maintain urine output and block ADH secretion o 200 to 300 mL of 3% NSS slowly and steadily increase Na; too rapid a rise may cause cerebral edema MIO, vital signs, weight, watch out for hyponatremia, serum and urine osmolality

V.

THYROID GLAND A. Hormones 1. Thyrocalcitonin or calcitonin decreases serum calcium level by transporting calcium from the blood to the bones 2. T3 triiodothyronine; more active; for cellular metabolism 3. T4 tetraiodothyronine; thyroxine; for thermogenesis ** T3 and T4 are synthesized from Iodine and Tyrosine Endocrine Disorders of the Thyroid gland 1. HYPOTHYROIDISM a. Types: By age: o Children: CRETINISM o Adults: MYXEDEMA Location of dysfunction o Primary or Thyroidal Hypothyroidism Problem on the thyroid gland itself Inc. TRH, inc. TSH, dec. T3 & T4 o Central Hypothyroidism Secondary or Pituitary Hypothyroidism Inc. TRH, dec. TSH, dec. T3 & T4 Tertiary or Hypothalamic Hypothyroidism Dec. TRH, dec. TSH, dec. T3 & T4 b. Three basic concepts: Dec. T3 = dec. metabolic rate Dec. T4 = dec. body heat production Inc. calcitonin = inc. serum calcium level dec. neuromuscular activity c. Assessment: Slowed physical and mental reactions Apathy, dull/expressionless/masklike face Generalized puffiness and edema around the eyes and face (myxedema) Enlarged tongue, slow speech, husky or hoarse voice Goiter may or may not be present Bradycardia, hyperlipidemia, atherosclerosis

B.

3.

SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE (SIADH) a. Hypersecretion of ADH caused by trauma, stroke, malignancies (often in the lungs or pancreas), medications, and stress b. Assessment: Water retention (fluid volume overload) Urine osmolality increases Urine specific gravity increases Weight gain Dilutional Hyponatremia / water intoxication Serum osmolality decreases

d.

e.

Anorexia, obesity, constipation, weight gain Irregular menstruation (menorrhagia, amenorrhea) Cold intolerance; subnormal temperature; coarse, dry, sparse hair; brittle nails, dry skin Extreme fatigue Hypoactive reflexes, weakness, muscle aches, paresthesias Inc. sensitivity to ANTS (anesthetics/analgesics, narcotics, tranquilizers, sedatives) = depressed respi drive alveolar hypoventilation progressive CO2 retention narcosis, coma (MYXEDEMA COMA) MYXEDEMA COMA extreme severe stage of hypothyroidism characterized by HYPOTHERMIA & UNCONSCIOUSNESS hypotension, bradycardia, hypothermia, hyponatremia, hypoglycemia, generalized edema, respiratory failure, coma precipitated by infection or other systemic disease or by sedatives, opioid analgesics, anesthetics, rapid withdrawal of thyroid medication supportive care for myxedema coma o ABG, pulse oximetry (hypercapnia, hypoxia, metabolic acidosis) o Assisted ventilation, oxygen; maintain patent airway; aspiration precaution o IV thyroid hormones (levothyroxine) o IV fluids (NSS or hypertonic as prescribed), glucose, corticosteroids o Avoid hypnotics, sedatives, analgesics o Keep patient warm o Monitor temperature hourly, BP frequently, changes in mental status, electrolyte and glucose levels Management: Orient patient to time, place, date, events Provide stimulation through conversation Explain meds: o proloid (Thyroglobulin) o dessicated thyroid extract o cytomel (Liothyronine) check BP, PR before admin.; start with low dose and gradually increase o levothyroxine (Synthroid) increases blood glucose level watch out for ANGINA or DYSRHYTHMIAS: Hypothyroid patients have subnormal metabolism and thus can tolerate a reduction of blood supply and relatively little O2. They are almost certain to have increased cholesterol, CAD, and atherosclerosis. Once levothyroxine therapy is started, it increases O2 demand and enhances cardiovascular effects of catecholamines instruct patient to report tachycardia, chest pain, restlessness, nervousness, insomnia, sweating, extreme weight loss (signs of overdose or hyperthyroidism) take the same time each day (AM) without food monitor V/S, including heart rate and rhythm high fiber, low calorie, low fat diet increase fluids within restriction (give fluids cautiously may cause water intoxication)

encourage mobility use laxatives and stool softeners sparingly encourage weight loss, weigh patient daily provide warm environment (extra blankets or clothing; warm room) avoid exposure to cold and drafts monitor body temperature avoid external heat source (heating pads, electric or warming blankets) space activities to promote rest and exercise as tolerated assist in self-care activities when patient is fatigued monitor patients response to increasing activities Avoid sedatives and opioid analgesics because of increased sensitivity to these medications.

2.

HYPERTHYROIDISM a. GRAVES DISEASE is the most common cause of hyperthyroidism b. Three basic concepts: Inc. T3 = inc. metabolic rate Inc. T4 = inc. body heat production Inc. calcitonin = dec. serum calcium level inc. neuromuscular activity c. Assessment: Irritability, agitation, mood swings, difficulty in concentrating, nervousness, cannot sit or stand still, hyperexcitable, apprehensive, fine tremors of the hands Exophthalmus, corneal injury Goiter enlargement of the thyroid gland Inc. PR, tachycardia, palpitations, hypertension Diarrhea, inc. appetite, progressive weight loss Amenorrhea Heat intolerance, fine tremors, shaky handwriting, clumsiness Diaphoresis; warm, soft, moist skin; fine, silky hairs, pliable nails Hyperactive reflexes d. THYROID STORM stress, infection, surgery, manipulation of the thyroid gland, overdose of thyroid medications ELEVATED TEMPERATURE (fever) initial sign Inc. BP, RR, CR; dysrhythmias, systolic hypertension, nausea, vomiting, diarrhea, tremors, anxiety, restlessness, agitation, confusion, seizures, delirium, psychotic state, coma Thyroid storm management: o Monitor V/S, MIO, neuro and CV status o Maintain a patent airway and adequate ventilation o Administer PTU, Iodide, propranolol, dexamethasone, glucocorticoids o O2 as needed o Maintain quiet, calm, cool, private environment o Lower fever (cooling devices, cold baths, acetaminophen) o Dont use ASA releases T3 & T4 e. Management: Provide rest, non-stimulating and cool environment (no loud music, conversation, or alarms) Promote safety Administer sedatives as ordered

Avoid stimulants Use calm, unhurried approach Monitor level of consciousness Suggest sunglasses to protect eyes from light Frequently moisten the conjunctiva with eye drops Improve self-esteem, address body image disturbance Mirrors may be covered or removed Avoid bringing physical changes to the patients attention Avoid excessive palpation of the thyroid to prevent THYROID STORM Monitor the ECG for arrhythmias Administer propranolol (Inderal) for tachycardia High calorie, high protein diet Monitor weight of the patient Balanced diet; small, frequent feedings (to 6x a day) Replace fluids lost through diarrhea and diaphoresis Avoid highly seasoned foods and stimulants A quiet environment during mealtime may aid digestion Provide cool and quiet environment Cool baths, cool/cold drinks may provide relief MIO, ensure adequate hydration and fluid balance Promote safety and improve self-esteem Drugs: o Beta-blockers for tachycardia o Calcium-channel blockers o Dexamethasone inhibits action of thyroid hormones o Iodides: LUGOLS SOLUTION (SSKI) Decreases release of thyroid hormones and the vascularity and size of the thyroid gland Used pre-thyroidectomy Mix with fruit juice with ice or glass of water Provide drinking straw Side-effects: allergic reaction, increased salivation Monitor for IODISM vomiting, abdominal pain, rash, sore gums and salivary glands, metallic or brassy taste in the mouth o Propylthiouracil (PTU) and methimazole (Tapazole) Inhibits synthesis of thyroid hormones Do not interfere with release or activity of previously formed T3 & T4 Take with meals to avoid GI upset Side-effect: AGRANULOCYTOSIS (fever, sore throat, rashes) o Radioactive iodine therapy Radioiodine is concentrated in the thyroid cells and destroys these cells Tasteless, colorless oral dose Body secretions will be radioactive; isolation for few days Not done to pregnant women; pregnancy delayed for 6 months after therapy Initially can cause an acute release of thyroid hormones: watch out for THYROID STORM

THYROIDECTOMY o Preop: maintain a EUTHYROID state Administer iodides, antithyroid agents, propranolol to prevent thyroid storm ECG, V/S, weight, electrolytes, monitor for hyperglycemia Instruct on DBCT exercises o Postop: Monitor for respiratory distress SEMI-FOWLERS with head, neck and shoulder erect Watch out for complications: Hemorrhage ice collar over the neck Check dressing anteriorly and at the back of the neck Airway obstruction monitor for respi distress (may be due to laryngobronchospasm) Have tracheostomy set, O2, suction at bedside Tetany (Hypocalcemia) Monitor BP for Trousseaus sign Keep calcium gluconate ready at bedside Recurrent laryngeal nerve damage AEB respi obstruction, dysphonia, high-pitched voice, stridor, dysphagia, restlessness Limit client talking Ask patient to speak every hour Thyroid storm Monitor body temperature

VI. PARATHYROID GLANDS A. Hormone / function: 1. Parathyroid hormone or parathormone or PTH secreted in response to decreased serum calcium level 2. PTH, therefore, increases serum calcium level by transporting calcium from the bones to the blood Endocrine disorders of the parathyroid glands: 1. HYPOPARATHYROIDISM a. Decreased secretion of PTH: HYPOCALCEMIA and HYPERPHOSPHATEMIA b. Assessment: Latent signs and symptoms: o Numbness, tingling, cramps in the extremities, stiffness of the hands and feet Overt signs and symptoms: o Bronchospasm, laryngospasm, carpopedal spasm, dysphagia, photophobia, cardiac dysrhythmias, seizures Other signs and symptoms: o Anxiety, irritability, depression, delirium, hypotension, ECG changes c. Management: Hypoparathyroidism after thyroidectomy: CALCIUM GLUCONATE o Caution in cardiac patients or those taking digitalis o If tetany and seizure activity do not subside after calcium gluconate is taken, PENTOBARBITAL can be used

B.

2.

Parenteral PTH only during acute episodes o Monitor for allergic reactions and serum calcium level Provide an environment free from noise, drafts, bright lights or sudden movements; SEIZURE PRECAUTIONS Watch out for RESPI DISTRESS o Have tracheostomy set, mechanical ventilator, bronchodilators ready Increase calcium and decrease phosphorus in the diet o NO milk, milk products, and egg yolk contain high level of P o NO spinach contains OXALATE which would form insoluble calcium substances Supplement calcium in the diet Amphojel to decrease P Vitamin D preparations Wear Medic-Alert bracelet

Inform that talking may be painful for 1-2 days postop Postop same with thyroidectomy

VII. ADRENAL GLANDS aka SUPRARENAL GLANDS A. ADRENAL CORTEX 1. Layers of the adrenal cortex: a. Zona glomerulosa b. Zona fasciculata c. Zona reticularis 2. Hormones of the adrenal cortex: STEROID HORMONES a. ALDOSTERONE produced by zona glomerulosa Causes sodium and water retention (Salt) b. GLUCOCORTICOIDS produced by zona fasciculata Increases blood sugar level (Sugar) c. ANDROGENS produced by zona reticularis Affects sex characteristics, personality and mood (Sex) ***Aldosterone, glucocorticoids, and androgens help the body to adapt to all kinds of stress ***Without AGA, there will be circulatory shock and collapse ***main stimulus for aldosterone secretion: PRESENCE OF ANGIOTENSIN 2 IN THE BLOOD (RAAS) ***minor stimulus for aldosterone secretion: ACTH ***main stimulus for glucocorticoid and androgen secretion: ACTH ADRENAL MEDULLA 1. The middle or inner part of the adrenal glands 2. Part of the sympathetic nervous system 3. Secretes catecholamines

HYPERPARATHYROIDISM a. Increased secretion of PTH: HYPERCALCEMIA and HYPOPHOSPHATEMIA b. Assessment: May be asymptomatic Irritability, neurosis to psychosis, apathy Hypertension, cardiac dysrhythmias Anorexia, nausea, vomiting, epigastric pain, constipation Fatigue, muscle weakness Bone decalcification (bone pain and tenderness) Risk for fractures Risk for renal calculi c. HYPERCALCEMIC CRISIS life-threatening neurologic, CV, and renal symptoms Management: IVF for rehydration, diuresis to decrease calcium level, calcitonin + corticosteroids, dialysis, pamidronate, etidronate (Didronel) d. Management: Education may suspect as psychosomatic Hydration: o Increase oral fluid intake (greater than or equal to 2L/day) o IV NSS o MIO o Cranberry juice to acidify urine o Prevent Dehydration (vomiting, diarrhea) to avoid hypercalcemic crisis o No thiazide diuretics decreased excretion of calcium Monitor V/S, especially BP, cardiac dysrhythmias Monitor calcium and phosphorus levels Diet and medications: o Avoid diet with restricted or excess calcium o Prune juice, stool softeners, physical activity, inc. OFI o Oral phosphorus, calcitonin Mobility o Move client slowly and carefully o Encourage walking or rocking chair o NO BED REST increased calcium excretion renal calculi Prepare and care for PARATHYROIDECTOMY o Preop monitor electrolytes (Ca, P, Mg) Ensure calcium levels are decreased to near normal values

B.

C. Endocrine disorders of the Adrenal glands 1. ADDISONS DISEASE a. Otherwise known as ADRENOCORTICAL INSUFFICIENCY b. Hyposecretion of AGA c. Assessment: Dec. Aldosterone: o Hyponatremia o Water loss o Hyperkalemia muscle weakness and fatigue o hypercalcemia o Weight loss o emaciation Dec. Glucocorticoid: o Hypoglycemia o Weakness, fatigue o Mental status changes o Anorexia o GI symptoms Dec. Androgens: o Emotional lability o Hair loss o Dec. hair growth o Menstrual changes in females o Impotence in males Dark pigmentation of skin, knuckles, elbows, mucous membranes due to inc. secretion of MSH Inability to cope with stress hypotension, risk for circulatory shock d. ADDISONIAN / ADRENAL CRISIS Due to overexertion, exposure to cold, acute infections, dec. salt intake, stress of surgery, dehydration from preop prep, abrupt withdrawal of steroid drugs

e.

Signs and symptoms of shock (dec. BP, inc. PR, inc. RR) Cyanosis, pallor Apprehension, confusion, restlessness Severe headache; severe abdominal, leg, and lower back pain Nausea, diarrhea, abdominal pain Management: o Restore blood circulation MODIFIED TRENDELENBURG POSITION o Maintain bed rest and provide a quiet environment o Corticosteroids and fluids HYDROCORTISONE SODIUM SUCCINATE (Solu-Cortef) IV, then followed by D5NS (glucose and sodium) o Vasopressors o Monitor V/S (BP), fluid status, neuro status o Antibiotics Management: Monitor V/S (BP), weight, I&O Monitor blood glucose and potassium level CORTISONE or HYDROCORTISONE o A synthetic glucocorticoid o Watch out for S/S of Cushings syndrome (hyperglycemia, hypertension, weight gain, etc.) o Decreases potassium; use K-sparing diuretics to relieve water retention o High K foods in the diet o Decreases calcium can lead to osteoporosis o DONT STOP ABRUPTLY can lead to ADDISONIAN CRISIS o An immunosuppressant avoid individuals with infections o Causes GI irritation administer after meals or with antacids ORAL FLUDROCORTISONE (FLORINEF) o A synthetic mineralocorticoid o Prevents dangerous dehydration, hypotension, hyponatremia, hyperkalemia o Give High K foods as it decreases K o Take with food or milk o Decreases K and Ca hypernatremia, water retention, osteoporosis, weight gain, heart failure o DO NOT STOP ABRUPTLY Client education: o Avoid individuals with an infection o High protein and high carbohydrate, normal sodium intake in the diet o Avoid strenuous exercise and stressful situations o Avoid over-the-counter medications o Wear a Medic-Alert bracelet

c.

o hypocalcemia Inc. Glucocorticoids: o Hyperglycemia o Protein catabolism Loss of muscle mass Thin extremities Bleeding, ecchymosis Fragile skin - striae Inc. Androgens: o Virilization o Hirsutism o Breast atrophy o Amenorrhea o Clitoris enlargement o Voice deepening o Loss of libido o Gynecomastia o Mood swings Suppressed inflammatory response increased susceptibility to infections Management: Monitor V/S (BP), I&O, weight Monitor blood sugar level MIO, weigh daily, monitor for edema Monitor WBC, Na, K, Ca Observe hypertensive patients who also have cardiac disease Watch out for infections High CHON, high K, low calories, low CHO, low Na diet Careful passive ROM if with osteoporosis Balance rest and activity Provide meticulous skin care Chemotherapy for inoperable adrenal tumors Radiation if caused by pituitary adenoma Prepare client for hypophysectomy Prepare client for adrenalectomy if caused by adrenal adenoma

3.

2.

CUSHINGS DISEASE and CUSHINGS SYNDROME a. Hypersecretion primarily of the glucocorticoids and androgen, although mineralocorticoids may also be increased b. Assessment: Inc. Aldosterone: o Hypernatremia o Water retention o Weight gain o Hypertension o Truncal obesity o Moon face o Buffalo hump o Hypokalemia

PRIMARY HYPERALDOSTERONISM / CONNS SYNDROME a. Hypersecretion of aldosterone, usually caused by adrenal tumor b. Assessment: Hypernatremia o Water retention o Increased blood volume o Hypertension o Increased serum osmolality o polydipsia Hypokalemia o Headache, muscle weakness, cramping, fatigue o Inability of kidneys to concentrate or acidify urine, polyuria, nocturia, polydipsia, dec. urine specific gravity o Interference with insulin secretion from pancreas, glucose intolerance Decreased hydrogen ions o Increased blood pH and bicarbonate o Metabolic alkalosis Hypokalemic alkalosis o Hypocalcemia tetany, paresthesias Visual changes c. Management: Monitor V/S (BP), hypokalemia, hypernatremia, I&O, urine specific gravity Spironolactone for hypertension K supplements Na restriction preoperatively Adrenalectomy hypokalemia resolves but hypertension may persist

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Glucocorticoids preoperatively to prevent adrenal hypofunction Monitor for adrenal insufficiency postoperatively Instruct client regarding need for glucocorticoid therapy following adrenalectomy Wear a Medic-Alert bracelet

B.

PHEOCHROMOCYTOMA a. Catecholamine-releasing adrenal medullary tumor b. Extra-adrenal tumor sites: Chest, Abdomen, Bladder, Brain c. Typically benign but can be malignant d. Diagnosis: VANNILYLMANDELIC ACID (VMA) TEST Avoid coffee, tea, cola, chocolate, bananas, vanilla, aspirin Specimen: 24-H urine collection Normal: up to 14 mcg/100mL of urine (+) Pheochromocytoma: >14mcg/100mL of urine e. Assessment: Triad of pheochromocytoma: o Headache o Diaphoresis o Palpitations Tremors, flushing, anxiety, hyperglycemia Chest or abdominal pain with nausea and vomiting Heat intolerance Weight loss 5 Hs: o Hypertension o Headache o Hyperhidrosis o Hypermetabolism o hyperglycemia f. Complications: Acute renal failure Cardiac dysrhythmias Aneurysms Stroke g. Management: Monitor V/S (BP, HR) Avoid increased abdominal pressure and vigorous abdominal palpation Avoid smoking, drinking caffeine-containing beverages Bed rest with HOB elevated to promote orthostatic decrease in BP, change position slowly Provide nonstressful environment Monitor blood glucose level Provide a diet high in calories, vitamins, and minerals Alpha-1 blockers: phentolamine (Regitine) Beta-blockers Smooth muscle relaxants: Na nitroprusside (Nipride) Primary treatment is Adrenalectomy

Endocrine function 1. The endocrine function of the pancreas is concentrated in the islets of Langerhans 2. The islets of Langerhans are composed of 3 major types of cells: a. Alpha cells produces GLUCAGON (increases blood sugar level) b. Beta cells produces INSULIN (decreases blood sugar level by transporting blood glucose into the cells to serve as cellular fuel or energy) c. Delta cells produces SOMATOSTATIN (regulates blood sugar level by suppressing the release of glucagon and insulin from the islets)

VIII. PANCREAS A. Exocrine function 1. Production and release of pancreatic enzymes to aid in digestion via the pancreatic duct into the duodenum: a. Amylase digests carbohydrates b. Trypsin digests proteins c. Lipase digests fats

C. DIABETES MELLITUS (DM) 1. Diagnostic criteria: a. FBS of > or equal to 126 mg/dL on 2 occasions b. RBS of > or equal to 200 mg/dL c. 2 PPBS of > or equal to 200 mg/dL 2. Types: a. Type I DM b. Type II DM c. GDM d. Secondary DM 3. TYPE I DM a. Formerly known as INSULIN-DEPENDENT DM or IDDM b. Juvenile in onset c. There is an absolute lack of insulin d. Due to immunologic, genetic, and environmental factors e. Cells do not receive source of energy f. Cells use proteins and fats to yield glucose for energy g. Usage of proteins cause muscles to be wasted and thinning of extremities and weight loss occur h. Usage of fats will yield fatty acids. Fatty acids accumulate in the blood, leading to hyperlipidemia and ultimately atherosclerosis i. Additionally, fat breakdown (lipolysis) leads to the formation of KETONE BODIES (acetone, acetoacetic acid, beta-hydroxybutyric acid) j. Ketone bodies are acidic and therefore can cause metabolic acidosis in the form of DIABETIC KETOACIDOSIS (DKA) k. DKA causes hyperventilation or KUSSMAULS RESPIRATIONS, and acetone breath 4. TYPE II DM a. Formerly known as NON-INSULIN DEPENDENT DM or NIDDM b. Adult in onset c. There is insulin resistance d. Due to obesity or lifestyle e. Cells may lack source of energy that is why the main problem is still hyperglycemia f. Hyperglycemia increases the osmolality of the blood g. No ketones are produced h. Can lead HHNS (HYPERGLYCEMIC HYPEROSMOLAR NONKETOTIC SYNDROME) i. May be given Oral Hypoglycemic Agents (OHA) j. Insulin may also be given especially in times of stress, surgery, illness, and pregnancy 5. Pathophysiologic changes a. The main problem with DM is HYPERGLYCEMIA. b. Hyperglycemia can lead to: Cellular starvation o Polyphagia o May lead to CHON and fat breakdown o CHON breakdown leads to muscle wasting and weight loss o Fat breakdown leads to hyperlipidemia, atherosclerosis and DKA

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Increased blood osmolality, which may cause: o Increased blood viscosity Sluggish circulation Dec. tissue perfusion Proliferation of microbes Degenerative or destructive changes (Complications of DM) Recurrent infections Poor wound healing o Increased osmotic pressure of the blood Increased osmotic pull of fluid out of the ICF compartment Cellular dehydration Polydipsia Can lead to HHNS and HHNComa (when brain cells are dehydrated, LOC will decrease and coma may ensue) A glucose level that is more than the renal threshold (normally 180-200 mg/dL only) o Glucose may leak out into the urine: GLUCOSURIA / GLYCOSURIA o Glycosuria increases the osmotic pressure of the urine o Osmotic pull of glucose in the urine increases the fluid content of the urine: OSMOTIC DIURESIS o This can lead to Polyuria and ECF DHN o Can lead to Polydipsia Management: NEMPE a. Nutrition Caloric distribution: o CHO = 50% to 60% o CHONS = 10% to 20% o Fats = up to 30% Alcohol consumption o Take in moderation o Can decrease blood glucose level o Take with food o Drink low-calorie or less sweet drinks (light beers or dry wine) Sweeteners o Take in moderation o Nutritive sweeteners provide calories same with sucrose but less elevation in blood sugar than sugar Ex. Fructose, sorbitol, xylitol ***sorbitol has a laxative effect o Non-nutritive sweeteners provide minimal or no calories Ex. Saccharin, aspartame, acesulfameK, sucralose (Splenda) ***sucralose (Splenda) is 600 times sweeter than sugar Be wary of misleading food labels like sugarless, sugar-free, dietetic, health food b. Exercise Initially can increase blood sugar level Net effect is lowering of blood sugar level Do not exercise if blood glucose level is greater than 250mg/dL or urine tests positive for the presence of ketones Do not overexert or do unusual exercise c. Monitoring Self-monitoring of blood glucose (SMBG) o Requires a finger prick to obtain a drop of blood for testing o Wash hands before and after performing the procedure to prevent infection o Follow the manufacturers instructions for the glucometer

d.

Check the expiration date on the test strips o If the blood glucose level results do not seem reasonable, reread the instructions, reassess technique, check the expiration date of the test strips, and perform the procedure again to verify results Urine testing for glucose not a reliable indicator of the blood glucose level and is therefore no longer used for monitoring purposes Urine testing for ketones should be performed during illness and whenever the client with type 1 DM has persistently elevated blood glucose levels (higher than 240 mg/dL for two consecutive testing periods) Glycosylated hemoglobin o Blood glucose bound to hemoglobin o Determines patients compliance within the last 3 to 4 months of therapy. o Fasting is not required o Values are expressed as a percentage of the total hemoglobin o Normal HbA1C for clients with DM is 4% to 6% o The goal for clients with DM is HbA1c of 7% or lower. o Elevated HbA1C means no compliance Pharmacology Insulin o Rapid-acting insulin onset of action starts within 10 to 15 min after administration Advise client to eat within 10 to 15 min after injection Ex. Lispro (Humalog) o Short-acting insulin CLEAR Ex. Regular insulin, semi-lente o Intermediate-acting insulin CLOUDY Ex. NPH (Neutral Protamine Hagedorn), lente o Long-acting insulin Ex. Ultralente o Very-long acting insulin Ex. Lantus (Glargine) o Onset, peak, and duration of shortacting, intermediate-acting, and longacting insulins Insulin Onset Peak Duration S -1H 2-4 H 6-8 H I 1-2 H 6-8 H 16-24 H L 2-4 H 16-24H 32-36 H ***The peak action time of insulin is important because of the possibility of hypoglycemic reactions occurring during that time Oral Hypoglycemic Agents (OHA) The following increases the hypoglycemic effect of OHA: Aspirin Alcohol Sulfonamides Oral contraceptives MAOI The following increases blood glucose level while taking with OHA: Glucocorticoids Thiazide diuretics Estrogen o Sulfonylureas stimulates the pancreas to release more insulin First-generation sulfonylureas: Less expensive o

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More CV effects Excreted only via the urine Shorter duration of action than 2nd generation sulfonylureas Increased frequency of administration May lead to poor compliance Ex. chlorpropamide (Diabinese) tolbutamide (Orinase) tolazamide (Tolinase) Second-generation sulfonylureas: More expensive Less CV effects Excreted via the urine and bile Longer duration of action than 1st generation sulfonylureas Decreased frequency of administration May lead to better compliance Ex. glipizide (Glucatrol) glyburide (Micronase) glimepiride (Amaryl) o Meglitinides stimulates the pancreas to release more insulin Ex. repaglinide (Prandin) o Biguanides Major effect: decreases hepatic synthesis of glucose Minor effect: increases peripheral uptake of glucose Ex. metformin (Glucophage) o Thiazolidinediones - Major effect: increases peripheral uptake of glucose Minor effect: decreases hepatic synthesis of glucose Ex. rosiglitazone (Avandia) pioglitazone (Actos) o Alpha-glucosidase inhibitor delays intestinal absorption of glucose Ex. acarbose (Precose) miglitol (Glyset) Education Insulin therapy o Regular insulin is the only insulin that can be administered intravenously o The following increases the hypoglycemic effect of insulin, causing a further decrease in the blood glucose level: Aspirin Alcohol Oral anticoagulants OHA Beta-blockers TCAs MAOIs o The following increases the blood glucose level: Glucocorticoids Thiazide diuretics Thyroid agents Oral contraceptives Estrogen o Illness, infection, and stress increase the blood glucose level and the need for insulin; insulin should not be withheld during illness, infection, or stress because hyperglycemia and ketoacidosis can result o Complications of insulin: Local and systemic allergic reactions Lipodystrophy (lipoatrophy and lipohypertrophy) Insulin resistance (due to obesity or antibody production against insulin)

Morning hyperglycemia Dawn phenomenon normal bld glucose until 3AM when growth hormone rises; the effect is increase in the bld glucose level in the morning Insulin waning progressive rise in bld glucose level from bedtime to morning as insulin levels in the body gradually decreases Somogyi phenomenon normal or elevated bld glucose level at bedtime, a decrease at 2-3AM to hypoglycemic levels; stress or counterregulatory hormones are released to compensate and the effect is increase in the bld glucose level in the morning Hypoglycemia Occurs when blood glucose level falls below 60 mg/dL or when the blood glucose level drops rapidly from an elevated level Mild hypoglycemia Client remains fully awake but displays adrenergic symptoms; bld glucose level is usually lower than 60 mg/dL Hunger, nervousness, palpitations, sweating, tachycardia, tremor Interventions: Give 10 to 15 g of a fast-acting simple carbohydrate (6-10 LifeSavers or hard candies, 4-6 oz. of fruit juice or soda, 34 commercially prepared glucose tablets, 2-3 tsp. of sugar or honey) Retest the blood glucose level in 15 mins and repeat the treatment if symptoms do not resolve Once the symptoms resolve, a snack containing protein and carbohydrates, such as milk or cheese and crackers, is recommended unless the client plans to eat a regular meal within 60 minutes Moderate hypoglycemia Client displays symptoms of worsening hypoglycemia; blood glucose level is usually lower than 40 mg/dL Confusion, double vision, drowsiness, emotional changes, headache, impaired coordination, inability to concentrate,

irrational or combative behavior, lightheadedness, numbness of the lips and tongue, slurred speech Interventions: Administer 15 to 30 g of a fast-acting simple carbohydrate Administer additional food such as low-fat milk or cheese after 10 to 15 minutes Severe hypoglycemia Client displays severe neuroglycopenic symptoms; blood glucose level is usually lower than 20 mg/dL Difficulty arousing, disoriented behavior, loss of consciousness, seizures Interventions: Notify the physician If the client is unconscious and cannot swallow, an injection of glucagon 1 mg is administered SC or IM Administer a second dose in 10 mins if the client remains unconscious Small meal is given when client awakens as long as he is not nauseated In the hospital or ER, the client may be treated with an IV injection of 25 to 50 mL of D50W Alternative methods of insulin delivery Insulin pens and disposable needles Using an prefilled insulin cartridge Jet injectors Delivers insulin through the skin under pressure in an extremely fine stream Bruising has occurred in some patients Insulin pumps 3mL syringe attached to a 24to 42-inch tube Needle/catheter is inserted to subcutaneous layer and secured with tapes Change needle/catheter at least every 3 days Pump worn on belt, pocket or bra Provides a continuous basal rate and the client delivers a bolus rate of insulin before each meal lispro (Humalog) and regular insulin are appropriate for use in these pumps Implantable insulin delivery An insulin pump is implanted in the peritoneal cavity, where

insulin can be absorbed in a more physiological manner Inhalant and transdermal (patch) insulin delivery under research o Storage Vial not in use: refrigerated Vial in use: room temperature to reduce local irritation at injection site Spare vials are considered vials not in use Avoid extremes of temperature o Cloudy insulin must be thoroughly mixed by gently inverting the vial or rolling in between palms of the hands before drawing o Mixing insulin into a syringe Injecting air into the vial: Inject air into the vial of the cloudy insulin first, then into the vial of the clear insulin Not withdrawing the syringe from the vial of the clear insulin, gently invert the vial of the clear insulin Withdrawing or aspirating the insulin: Withdraw or aspirate from the vial of the clear insulin first, followed by the vial of the cloudy insulin An easy way to remember this is through the mnemonic NR-RN (inject air into NPH [cloudy] first then into the Regular [clear]; withdraw/aspirate Regular [clear] first then the NPH [cloudy]) o Rotate injection sites within 1 anatomic site at a time Anatomic sites: abdomen, posterior aspect of the upper arms, hips, upper thighs Distance bet injection sites is 0.5 to 1 inch o Cleansing injection site with alcohol is not a must. If alcohol was used to cleanse injection site, let the applied alcohol dry first to prevent seepage of the alcohol into the injection site causing local irritation o Do not aspirate for blood Pancreas transplantation are performed on a limited number of clients (generally, these are clients who are undergoing kidney transplantation simultaneously); immunosuppressive therapy is prescribed to prevent and treat rejection Complications o Acute complications: Diabetic Ketoacidosis (DKA) Sudden in onset Precipitated by infection, stress, inadequate insulin dose Assessment: Hyperglycemia Dehydration: polyuria, polydipsia, weight loss, dry skin, sunken eyes, soft eyeballs, lethargy, coma Ketosis: kussmauls respiration, fruity/acetone breath, nausea, abdominal pain

Acidosis Interventions: Restore circulating blood volume and protect against cerebral, coronary, or renal hypoperfusion Rapid IV infusions of 0.9% or 0.45% NS D5NS or 5% dextrose in 0.45% saline when the blood glucose level reaches 250 to 300 mg/dL Administer IV regular insulin Monitor for potassium, glucose levels and for signs of increased ICP during insulin therapy If blood glucose level falls too far or too fast before the brain has to time to equilibrate, water is pulled from the blood to the CSF and the brain, causing cerebral edema and increased ICP K IV in a diluted solution as prescribed when K reaches a normal level to prevent hypokalemia Ensure adequate renal function before administering potassium Hyperglycemic Hyperosmolar Non-Ketotic Syndrome (HHNS) Gradual in onset Precipitated by infection, stress, and poor fluid intake Assessment: Major difference with DKA is that ketosis and acidosis do not occur Altered CNS function with neurologic symptoms Dehydration: polyuria, polydipsia, weight loss, dry skin, sunken eyes, soft eyeballs, lethargy, coma Interventions: Treatment is similar to that for DKA Fluid replacement, correction of electrolyte imbalances, insulin administration Insulin plays a less critical role in the treatment of HHNS than it does for the treatment for DKA because ketosis and acidosis do not occur; rehydration alone may decrease glucose levels Chronic complications: Microvascular complications: Diabetic retinopathy Description: Chronic and progressive impairment of the retinal circulation

that eventually causes hemorrhage Permanent vision changes and blindness can occur The client has difficulty with carrying out the daily tasks of blood glucose testing and insulin injections Assessment: A change in vision is caused by the rupture of small microaneurysms in retinal blood vessels Blurred vision results from macular edema Sudden loss of vision results from retinal detachment Cataracts result from lens opacity Interventions: Maintain safety Prevention by control of HPN and blood glucose levels Photocoagulation (laser therapy) removes hemorrhagic tissue to decrease scarring and prevent progression of the disease process Vitrectomy removes vitreous hemorrhages and thus decreases tension on the retina, preventing detachment Cataract removal with lens implantation improves vision Diabetic nephropathy Description: Progressive decrease in kidney function Assessment: Microalbuminuria Thirst Fatigue Anemia Weight loss Sings of malnutrition Frequent UTIs Sings of neurogenic bladder Interventions: Prevention by control of HPN and blood glucose levels Assess V/S, monitor I&O, serum BUN and crea, and urine albumin levels Restrict dietary protein, sodium, and potassium intake as prescribed

Avoid nephrotoxic drugs Prepare for dialysis, kidney transplant, pancreas transplant as prescribed Neuropathy Description: General deterioration of the nervous system throughout the body Complications include the development of nonhealing ulcers of the feet, gastric paresis, and erectile dysfunction Classifications: Focal neuropathy or mononeuropathy involves a single nerve or group of nerves, most frequently cranial nerves III and VI, resulting in diplopia; usually resolves spontaneously Sensory or peripheral neuropathy affects distal portion of nerves, most frequently in the lower extremities Autonomic neuropathy symptoms vary according to organ system involved Cardiovascular cardiac denervation syndrome (heart rate does not respond to changes in oxygenation needs) and orthostatic hypotension occur Pupillary pupil does not dilate in response to decreased light Gastric decreased gastric emptying (gastroparesis) Urinary neurogenic bladder Sudomotor: decreased sweating Adrenal hypoglycemic unawareness Reproductive impotence (male), painful

intercourse (female) Assessment: Paresthesias Decreased or absent reflexes Decreased sensation to vibration or light touch Pain, aching, and burning in the lower extremities Poor peripheral pulses Skin breakdown and signs of infection Weakness or loss of sensation in cranial nerves III, IV, V, and VI Dizziness and postural hypotension Nausea and vomiting Diarrhea or constipation Incontinence Dyspareunia Impotence Hypoglycemic unawareness Interventions: Prevention is by control of HPN and blood glucose levels Administer pain medications as prescribed Estrogen-containing lubricants for women with dyspareunia Careful foot care Inspect the feet daily Wash with warm water and mild soap Pat them dry do not rub Wear comfortable, properly-fitted pair of shoes Use white cotton socks Do not go barefooted Trim toenails straight across Do not cut the lateral edges ingrown may develop Exercise or massage the feet Do not wear knee-high or stay-up stockings Consult a Podiatrist for any injury

Macrovascular complications: Cerebrovascular diseases TIAs Stroke Cardiovascular diseases MI, usually silent due to accompanying autonomic neuropathy CAD Peripheral vascular diseases PAOD PVOD Management: Prevention and treatment of atherosclerosis Diet and exercise to manage obesity, HPN, and hyperlipidemia Smoking cessation Control of blood glucose levels Insulin May need to be increased during illnesses Client may need to switch from OHA to insulin during illnesses

RESOURCES: 1. 2. 3. 4. 5. Brunner & Suddarths Textbook of Medical-Surgical Nursing, 10th edition, Volume 2 Saunderss Comprehensive Review for the NCLEX-RN Examination, 4th edition Straight As in Pathophysiology by Lippincott Williams & Wilkins Straight As in Anatomy & Physiology by Lippincott Williams & Wilkins Medical-Surgical Nursing: Concepts and Clinical Application, 1st edition by Josie Quiambao-Udan, RN, MAN