You are on page 1of 7

ENDOCRINE GLANDS

PITUITARY GLAND Pituitary gland is a master gland. Located at the base of the brain. Directly affects the function of the other endocrine glands. Promotes growth of body tissues. Influences water absorption by the kidney. Controls sexual development and function. ADRENAL GLANDS Two small glands, one above each kidney. Regulates sodium and water retention. Affects CHO, fat and CHON metabolism. Influences development of sexual characteristics. The adrenal cortex synthesizes glucocorticoids and mineralocorticoids. The adrenal medulla produces epinephrine and norepinephrine. THYROID GLAND Located anterior part of the neck. Controls rate of body metabolism and growth. Produces T4, T3 and thyrocalcitonin. PARATHYROID GLANDS Located near the thyroid. Controls calcium and phosphorus metabolism. Produces parathyroid hormone. PANCREAS Located posterior of liver. Influences CHO metabolism. Indirectly influences fat and CHON metabolism. Produces insulin and glucagon. OVARIES Located in the pelvic cavity. Produce estrogen and progesterone. TESTES Located in the scrotum. Contributes to the development sex characteristics. Produce testosterone. PITUITARY GLAND (HYPOPHYSIS)

PROLACTIN (MAMMOTROPIC/ LACTOTROPIC HORMONE/ LUTEOTROPIC HORMONE)


development of mammary glands & lactation Hypersecretion- Galactorrhea Hyposecretion- Absence of milk during lactation

MSH (Melanocyte- Stimulating Hormone)


timulates adrenal cortex; affect pigmentation Hypersecretion- Eternal tan/ Bronze appearance of skin Hyposecretion- Albinism

Posterior Pituitary

ADH (Antidiuretic Hormone/Vasopressin)


regulates water metabolism; helps body to retain water. Hypersecretion- SIADH (Syndrome of Inappropriate Antidiuretic Hormone) Hyposecretion- Diabetes Insipidus

Oxytocin
stimulates uterine contractions during labor and milk secretion in lactating mothers.

DIAGNOSTIC TESTS
T3 & T4 RESIN UPTAKE TEST
o o o o Blood test for diagnosis of thyroid disorders T3 & T4 regulate thyroid-stimulating hormone Normal Value of T3: 80-230 mg/dL T4: 5-12 mg/dL Both values increase in hyperthyroidism & decreased in hypothyroidism

THYROID-STIMULATING HORMONE (TSH)


o Blood test used to differentiate the diagnosis of primary hypothyroidism from secondary hypothyroidism. Normal value is 0.2 to 5.4 mu/ml Elevated in primary hypothyroidism & decreased in hyperthyroidism or secondary hypothyroidism

o
o

THYROID SCAN
o o Performed to identify nodules or growths in the thyroid glands A radioisotope of iodine or technetium is administered prior to the scanning of the thyroid gland. A scanner is used to detect pattern of uptake of the thyroid gland. Level of radioisotope is not dangerous to self or others.

Anterior Pituitary

Follicle-Stimulating Hormone/ Luteinizing Hormone


stimulates graafian follicle growth and estrogen secretion. induces ovulation & development of corpus luteum and stimulates testosterone secretion in men. Hypersecretion- Precocious Puberty Hyposecretion- poor puberty development

NEEDLE ASPIRATION OF THYROID TISSUE


o o o Aspiration of thyroid tissue for cytological exam No preparation needed Light pressure applied to aspiration site after the procedure

ACTH (Adrenocorticotropic Hormone)


stimulates secretion of hormones from adrenal cortex. Hypersecretion- *Cushings Disorder Hyposecretion- *Addisons Disorder

Eight-hour intravenous ACTH Test


o o o Administration of 25 units of ACTH in 500 ml of saline over an 8-hr period. Used to determine function of adrenal cortex. In Addisons disease, urinary output of steroids does not increase following administration of ACTH; normally steroid excretion increases threefold to fivefold ff. ACTH administration. In Cushings syndrome, hyperactivity of the adrenal cortex increases the urine output of steroids in the second urine specimen tenfold.

TSH (Thyroid stimulating Hormone)


regulates secretory activity of thyroid gland. Hypersecretion- *Hyperthyroidism Hyposecretion- *Hypothyroidism

GH (Growth Hormone, Somatotropin)


stimulates growth of cells, bones, muscles and soft tissue. Hypersecretion- Children: Gigantism; Adults: Acromegaly Hyposecretion- Dwarfism

GLUCOSE TOLERANCE TEST (GTT)


o o Aids in the diagnosis of diabetes mellitus If the glucose level peaks at higher than normal at 1 to2 hours after injection or ingestion of glucose, and are slower than normal to return to normal levels, DM is diagnosed

GLYCOSYLATED HEMOGLOBIN
o o o o o Glycosylated hemoglobin is blood glucose bound to hemoglobin Is a reflection of how well blood glucose levels have been controlled for up to the prior 4 months Hyperglycemia in clients with DM causes increase in glycosylated hemoglobin Fasting is not needed Values: Diabetics with good control: 7.5% or less Diabetics with fair control: 7.6% to 8.9% Diabetics with poor control: 9% or greater

HYPERPITUITARISM Hypersecretion of the anterior pituitary gland which resulting in oversecretion of one or more of the anterior pituitary hormones. Overproduction of GH causing gigantism or acromegaly Gigantism occurs in childhood before the closure of epiphyses of the long bones vs acromegaly which occurs after the closure of epiphyses of the long bones Etiology: - Unknown, Pituitary adenomas/tumors Assessment Clinical Manifestation: o large hands & feet, o thickening & protrusion of jaw o arthritic changes, o visual disturbances, o diaphoresis, o oily and rough skin, o organomegaly, o hypertension o dysphagia, o deepening of voice o Neurologic headache, hemianopsia, signs and symptoms of ICP, behavioral changes seizures o Women irregular menses, amenorrhea, infertility, galactorrhea, dyspareunia, decrease vaginal lubrication, decrease libido Medical and Nursing Management o Emotional support; frequent skin care; pharmacologic & non-pharmacologic interventions for joint pains o Prepare for radiation of pituitary gland or removal of pituitary gland o Pharmacotherapy Bromocriptine (Parlodel) Decrease Growth Hormone levels Decrease prolactin levels NURSING DIAGNOSES o Disturbed body image (NR: ventilation of feelings, therapeutic communication) o Activity Intolerance (NR: provide rest; assist ADLs) o Chronic Pain (NR: provide diversional activity) o Knowledge deficit

Disorders of the Pituitary Gland


ANTERIOR PITUITARY
o o o o Hypopituitarism Hyperpituitarism Diabetes Insipidus SIADH (Syndrome of Inappropriate Antidiuretic Hormone

POSTERIOR PITUITARY

Anterior pituitary Gland


Hyper and Hypo secretion of growth hormone
Insufficient secretion during childhood results in generalized limited growth and dwarfism. Hypersecretion would result in Cushings syndrome or acromegaly.

HYPOPITUITARISM Hyposecretion of growth hormone by the anterior pituitary gland causing deficiencies both in the pituitary hormone and the target glands. Assessment Clinical Manifestation: o mild to moderate obesity, o reduced cardiac output, o infertility, o sexual dysfunction, o poor development of secondary sex characteristics o retarded physical growth, o low intellectual development, o fatigue, o low blood pressure, o tumors of the pituitary may also cause headaches and visual defect o o o o o Note: Causes: Disorders of pituitary Idiopathic Encephalitis Trauma Tumors

40% smaller than normal person; 20 y/o more or less (lifespan)

HYPOPHYSECTOMY
Is the removal of the pituitary gland via craniotomy or via transsphenoidal (endoscopic transnasal) approach. Complications for craniotomy o increased ICP, o bleeding, o meningitis o hypopituitarism Complication for transsphenoidal surgery o cerebrospinal fluid leak, o infection, o hypopituitarism. Post-operative care: o Monitor V/S, neurological status & LOC (Glasgow Coma Scale) o Elevate head of bed

Medical and Nursing Management Provide emotional support to client and family Encourage client family to express feelings related to altered body image or sexual dysfunction HRT Surgical Removal of the tumor Radiation NURSING DIAGNOSES o Disturbed body image o Sexual dysfunction related to hormonal imbalance o Imbalanced nutrition o Deficient Fluid Volume o Ineffective therapeutic regimen

o o o o o

Monitor for increased intracranial pressure & any postnasal drip which might be CSF Avoid sneezing, coughing & blowing nose Monitor for temporary diabetes insipidus Monitor I & O & water intoxication Administer antibiotics, analgesics, antipyretics, hormones & glucocorticoids if entire gland is removed

weight gain, hypertension, tachycardia, hyponatremia

Posterior Pituitary Gland


DIABETES INSIPIDUS Hyposecretion of ADH & deficiency of vasopressin Kidney tubules fail to reabsorb water Etiology: o by trauma, strokes, or idiopathic causes

Nursing management: Monitor I & O and daily weight; Monitor fluid & electrolyte balance; Restrict fluids as prescribed; Administer diuretics & monitor IV fluids carefully Meds: demeclocycline (Declomycin) inhibits ADH-induced water reabsorption & produces water diuresis NURSING DIAGNOSES Risk for injury Fluid Volume excess Imbalanced Nutrition Knowledge deficit

TYPES OF Diabetes Insipidus: Nephrogenic Diabetes Insipidus Inherited defect in the kidney Unable to respond to ADH Neurogenic Diabetes Insipidus Abnormal pituitary gland (causes decrease production of ADH) Dispogenic Diabetes Insipidus Abnormal thirst stimulation Gestational Diabetes Insipidus Occurs during pregnancy Assessment Clinical Manifestation: o polyuria; o polydipsia, o dehydration o decreased skin turgor, o dry mucus membranes, o dehydration, o constipation o concentrate urine, o low urine specific gravity o fatigue, o postural hypotension, o headache Nursing Management: Provide safe environment especially with decreasing LOC Monitoring I & O with specific gravity, Meds: o vasopressin tannate (Pitressin Tannate) o desmopressin acetate (DDAVP, Stimate) o lypressin (Diapid) Enhances reabsorption of water in the kidneys promoting antidiuretic effect & regulates fluid balance A/R: hypertension; nasal congestion NURSING DIAGNOSES Fluid Volume Deficit Activity Intolerance Imbalanced Nutrition Anxiety Knowledge deficit (SIADH) Syndrome of INAPPROPRIATE ANTIDIURETIC o Hypersecretion of ADH o Retains water in the renal tubules Causes: trauma, strokes, malignancies, medications (vincristine,phenothiazines, tricyclic antidepressants, thiazide diuretics, and others) stress Assessment: Clinical Manifestation: o Signs of fluid overload; changes in LOC & mental status;

Disorders of the Adrenal Gland


ADRENAL CORTEX
Addisons disease Cushings syndrome Aldosteronism (Conns Syndrome) Pheochromocytoma

ADRENAL MEDULLA

ADRENAL CORTEX
ADDISONS DISEASE
Hyposecretion of the adrenal cortex hormones (glucocorticoids and mineralocorticoids) ETIOLOGY: o Idiopathic atrophy (caused by an autoimmune abnormality) o infection, o congenital hypolplasia, o surgical removal of adrenal glands

Assessment: Subjective Muscle weakness, fatigue, lethargy, dizziness, fainting, nausea, anorexia, abdominal pain/cramps. Objective: V/S: decreased BP, orthostatic hypotension Pulse: increased, collapsing, irregular Subnormal temp. Vomiting, diarrhea, weight loss Tremors Skin: poor turgor excessive pigmentation (bronze tone) Hyponatremia, hypoglycemia, hyperkalemia NURSING MANAGEMENT: 1. Decrease stress 2. Promote adequate nutrition: o Diet o Fluids o Administer lifelong exogenous replacement therapy as ordered: Glucocorticoids- prednisone, hydrocortisone Mineralocorticoids- fludrocortisone (Florinef) 3. Health teaching: a. Take meds with food or milk. b. Avoid stress 4. Monitor for s/sx of addisonian crisis

ADDISONIAN CRISIS
Life-threatening disorder caused by acute adrenal insufficiency precipitated by stress, infection, trauma or surgery. May cause hyponatremia, hypoglycemia, hyperkalemia & shock. Given glucocorticoids IV e.g. hydrocortisone Na succinate (Solu-Cortef), mineralocorticoids e.g. fludrocortisone (Florinef). Severe, generalized muscle weakness, severe hypotension, hypovolemia, shock (vascular collapse) Check BP & electrolyte levels. Strict bed rest in quiet environment & protect from infection.

Clinical Manifestation: o HPN, o severe HEADACHE, o Palpitations, o pain in chest or abdomen, o hyperglycemia & glycosuria, o profuse sweating, o n/v, o dilated pupils, o tachycardia, o cold extremities. Nursing Management: o Monitor for hypertensive crisis & avoid stimuli which triggers it such as : increased abdominal pressure, vigorous abdominal palpation micturation o Instruct patient not to smoke, drink cola, coffee or tea o Monitor blood glucose & urine for glucose & acetone. HYPERTENSIVE CRISIS Life threatening Headache Blurred vision Diastolic pressure of 130mmhg (cardiac and renal damage)

Assessment: Subjective: headache, backache, weakness, decreased work capacity Objective: Hypertension, weight gain, pitting edema Characteristic fat deposits, truncal & cervical obesity (buffalo hump). Pendulous abdomen, purple striae, easy bruising Moon face, acne, hyperpigmentation, impotence Virilization in women: hirsutism, breast atrophy, amenorrhea Pathologic fractures reduced height Slow wound healing Hypernatremia, hyperglycemia, hypokalemia

ADRENALECTOMY
surgical removal of one or more of the adrenal gland because of tumors or overactivity; Preop: reduce risk of postop cx o Prescribed steroid therapy, given 1 wk. before surgery o Antihypertensive drugs discontinued o Sedation as ordered During surgery: monitor for hypotension & hemorrhage Postop: promote hormonal balance o Administer hydrocortisone o Monitor for signs of Addisonian crisis Observe for hemorrhage and shock. Prevent infection. Administer cortisone or hydrocortisone as prescribed.

HYPERALDOSTERONISM (CONNS SYNDROME)


Hypersecretion of aldosterone from the adrenal cortex of the adrenal gland commonly caused by adenoma Signs and symptoms: o hypertension, o hypokalemia, o headache, o polydypsia o polyuria, o hypernatremia, o low urine specific gravity Management Monitor I & O & administer spironolactone (Aldactone) & Potassium Supplements & maintain Na restriction Administer antihypertensives as px Usually will be undergoing adrenalectomy; administer glucocorticoids pre & post-op.

ADRENOCORTICOTROPHIC HORMONES
Dethamethasone (Celestone), cortisone (Cortone) dexamethasone (Decadron), prednisone (Orasone) Stimulate the adrenal cortex to secrete cortisol Produces an antiinflammatory effect. Adverse reaction: Increased appetite, mood swings, water & Na retention, hypocalcemia & hypokalemia, cushing-like symptoms o Check I & O, weight and for edema (decrease Na intake) o Monitor for infection o Monitor electrolyte & calcium levels o Monitor for poor wound healing, menstrual irregularities,decrease in growth & edema o Dose must be tapered & not stopped abruptly -

PHEOCHROMOCYTOMA
Catecholamine-producing tumor usually found in the adrenal gland.

CORTICOSTEROIDS (GLUCOCORTICOIDS)
Produce metabolic effects; alters normal immune response & suppress inflammation; promote Na & H2O retention & K+excretion Produce antiinflammatory , antiallergic & anti-stress effects; replacement for adrenocortical insufficiency A/R: hyperglycemia, hypokalemia, edema & masks signs & symptoms of infection C/I: DM, increases effect of anticoagulants & oral antidiabetic agents; increases potency of aspirins & NSAIDS & K-sparing diuretics Check for overdose or signs of Cushings syndrome; additional doses during stress or surgery.

Complications: o hypertensive retinopathy, caused by constant increase in BP o CVA & CHF

5 H:
HYPERTENSION HYPERMETABOLISM HYPERHIDROSIS HEADACHE HYPERGLYCEMIA

MINERALOCORTICOIDS FLUDROCORTISONE (FLORINEF)


Steroid hormones that enhance the reabsorption of NaCl & promote K+ excretion & hydrogen at the renal tubule promoting fluid & electrolyte balance Used in primary & secondary Addisons disease S/E: o Na/H2O retention, o hypokalemia, o hypocalcemia, o delayed wound healing, o increased susceptibility to infection, o mood swings, o weight gain Take with food or milk; high-K+ diet

NURSING DIAGNOSES: Activity intolerance Imbalanced nutrition more than body requirements Hypotension Constipation Disturbed body image Risk for impaired skin integrity Decreased cardiac output Anxiety Self care Note: o o Children: Cretinism Adult: Myxedema

DISORDERS OF THE THYROID GLAND


HYPOTHYROIDISM
Hyposecretion of the thyroid hormone characterized by decrease rate of body metabolism. o Etiology autoimmune thyroiditis, ablative therapy, and idiopathic Assessment: Subjective data: Weakness, fatigue, lethargy, headache, slow memory, loss of interest in sexual activity. Objective data: o Depressed BMR; intolerance to cold o Cardiomegaly, bradycardia, hypotension, anemia o Menorrhagia, amenorrhea, infertility o Dry skin, brittle nails, coarse hair, hair loss o Slow speech, hoarseness, thickened tongue o Weight gain: edema, periorbital puffiness o Lab data: elevated TSH; normal-low serum T4 & T3; decreased RAUI. o

Cretinism (manifestation)
o o o o o Dull expression Lack of coordination Smaller than normal Arrested physical growth Mental retardation

MYXEDEMA COMA
Rare but serious d/o which result from persistently low thyroid hormone precipitated by acute illness, rapid withdrawal of thyroid meds, use of sedatives & narcotics Manifestation: o Facial puffiness o Puffy eyelids o Swelling of limbs and abdomen o Mental dullness o Slowed metabolism Assessment: o hypotension, o bradycardia, o hypothermia, o hyponatremia, o hypoglycemia, o respiratory failure Management: Patent airway Keep patient warm & check V/S frequently Administer IV fluids & levothyroxine Na (Synthroid) Give IV glucose & corticosteroids

THYROID HORMONES
Levothyroxine (Synthroid, Levothroid, Levoxyl) Thyroglobulin (Proloid) o Controls the metabolic rate of tissues & accelerates heat production & oxygen consumption o For hypothyroidism, myxedema & cretinism o A/R: cramps, diarrhea, nervousness, tremors, hypertension, tachycardia, insomnia, seating & heat intolerance o Taken same time every day preferably in the a.m. with food o Teach client to how to take HR o Avoid foods that will inhibit thyroid secretions

HASHIMOTOS THYROIDITIS
Also known as Lymphocytic Thyroiditis A chronic progressive disease of the gland caused by the infiltration of lymphocytes believed to be an autoimmune disease; genetically transmitted and perhaps related to Graves disease Cause is unknown 95% of cases: women (40s or 50s) Possibly the most common cause of adult hypothyroidism Early phase: Goiter Late phase: Thyroid shrinks Assessment Clinical Manifestation: thyroid is firm and smooth, moves freely, painless Periods of hyper and hypoparathyroidism. Nursing Management: patient teaching related to progress of the disorder thyroid hormone replacement Surgery if the goiter is unresponsive to thyroid hormone.

Hypothyroidism
Nursing management Monitor HR including rhythm. Instruct patient for: thyroid replacement therapy Diet Assess for constipation Provide for warm environment. Monitor for overdose of thyroid meds. Note: o Diet: Soft diet Low caloric Low cholesterol High fiber Low fat

Hyperthyroidism Hypersecretion of the thyroid hormone T3, T4,


Thyrocalcitonin Provide cool and quiet environment

Photosensitivity; unable to close eyelids Etiology: o benign adenomas, Graves disease o frequently in adults between ages 20 and 50 o 2 to 4x common in women 3 concepts occur in hyperthyroidism: T3 increased metabolic rate T4 increased body heat pressure Thyrocalcitonin - hypocalcemia DIET:

THYROID STORM
Acute & life threatening condition in uncontrolled hyperthyroidism Risk factors: o Infection, o surgery, o beginning labor to give birth, o Taking inadequate antithyroid medications before thyroidectomy.

High caloric High protein Low cholesterol

NURSING DIAGNOSES Decreased cardiac output ( due to cardiac stress) Activity intolerance Disturbed sleep pattern Hyperthermia Imbalanced nutrition less than body requirements Risk for injury Disturbed sensory perception

Assessment: fever, tachycardia, hypotension, marked respiratory distress, pulmonary edema, irritability, apprehension, agitation, restlessness, confusion, seizures Nursing Management: maintain patent airway and adequate ventilation, monitor V/S monitor for cardiac dysrythmias, use cooling blanket to dec. temp. MEDICAL MANAGEMENT: 1. Propylthiouracil (PTU) o blocks thyroid synthesis 2. Methimazole (Tapazole) o to inhibit synthesis of thyroid hormone 3. Iodine preparations (SSKI, Lugols Solution) o decrease size & vascularity of the thyroid gland o palatable if diluted with water, milk or juice o give through straw tp prevent staining of teeth o takes 2-4 weeks before results are evident 4. Beta blockers: Propranolol (Inderal), atenolol (Tenormin), metoprolol (Lopressor) o given to counteract the increased metabolic effect of thyroid hormones o relieve symptoms of tachycardia, tremors & anxiety

GRAvES DISEASE
Most common cause of hyperthyroidism (75% of cases) Occurs most frequently between 20 and 40 years of age Seen worldwide, incidence correlated with amount of iodine in diet Precipitated by stress, infections, genetic factors

Assessment: o Goiter: thyroid gland noticeable & palpable o Gyne: abnormal menstruation o GI: frequent bowel movements o Activity pattern: fatigue which leads to depression o Lab data: elevated T3 & T4 level; elevated RAIU; elevated metabolic rate (BMR); decreased WBC caused by decreased granulocytosis (<4500). Note: EXOPTHALMOS due to: o Edema o Fat deposits NR: provide sunglasses

THYROIDECTOMY
Removal of thyroid gland & performed for persistent hyperthyroidism PRE-OPERATIVE CARE: o Assess V/S, weight, electrolyte & glucose level o Teach DBE & coughing as well as how to support neck in post-op period when coughing & moving o Administer antithyroid meds etc. to prevent thyroid storm POST-OP CARE: o Monitor for respiratory distress o Maintain semi-Fowlers position to reduce edema o Immobilize head with pillows/sandbags; -Check surgical site for edema & bleeding o Limit client talking & assess for hoarseness o Assess for laryngeal nerve damagehigh-pitched voice, stridor, o Monitor for signs of hypocalcemia & tetany & have calcium gluconate at bed side At bedside: Oxygen Suction Tracheostomy set Avoid flexion and hyperextension Laryngeal damage: (check for) Dysphagia Dysphonia Restlessness o

TOXIC MULTINODULAR GOITER


Slower to develop than Graves disease Characteristic massive enlargement of neck (goiter)

NURSING MANAGEMENT o Protect from stress: private room, restrict visitors, quiet environment. o Promote physical & emotional equilibrium o Prevent complications o Monitor for thyroid storm. o Health teaching: stress reduction techniques; importance of medications; methods to protect eyes from environment; s/sx of thyroid storm. Note: o IODINE Synthesize thyroid hormone o GOITROGENS: Peas Cauliflower Cabbage Turnips Spinach Peanut cover Radish Strawberry

stridor

renal stones

Disorders of the Parathyroid Gland


HYPOPARATHYROIDISM
o A condition which reflects deficient PTH secretion resulting in hypocalcemia and hyperexcitability o Etiologic Classifications Congenital absence of all the parathyroid glands Acquired deficiency Neck surgery (removal of parathyroid adenoma, thyroidectomy, bilateral neck resection for cancer) Malignancy or metastasis from a cancer to the parathyroid glands Infection Magnesium deficiency (magnesium regulates PTH release) Idiopathic autoimmune or familial origin Antiparathyroid antibodies found resistance to PTH action. May occur w/ other autoimmune d/o such as adrenal insufficiency, hypothyroidism, diabetes mellitus, pernicious anemia, vitiligo Clinical Manifestation: hypocalcemia, numbness and tingling in the face, muscle cramps and cramps in the abdomen or in the extremities, (+) trousseaus and chvosteks sign, signs of tetany, hypotension, anxiety, irritability, depression Note: SIGNS OF HYPOCALCEMIA (+) Chvosteks sign from A. Chvostek; Austrian surgeon facial twitching (+) Trousseaus sign from F. Trousseau; French carpal spasm flexion of the wrist abduction of the thumb Nursing Management: Monitor for hypocalcemia & institute seizure precautions Place a tracheostomy set, O2 & suction machine at bed side Prepare for calcium gluconate/chloride IV Provide high-calcium/low-phosphorus diet Give vitamin D to enhance calcium absorption at the GIT Given phosphate binders Wear medic-alert bracelet

Nursing Management: Encourage fluids & administer furosemide (Lasix) & IV salineas px Move patient slowly & carefully Administer phosphates as px Administer calcitonin (Calcimar) as px to decrease skeletal calcium release & increase renal calcium clearance & monitor for hypocalcemia & report to MD Prepare for parathyroidectomy

ParathyroidectomY

Removal of 1 or more parathyroid gland PRE-OPERATIVE CARE: monitor calcium, phosphate & magnesium level ensure that calcium is near normal explain to patient that talking may be painful 2 days post-op POST-OPERATIVE CARE: monitor for respiratory distress & have a tracheostomy set, O2 & suction machine at bed side Semi-Fowlers position Check for bleeding Check for hypocalcemic crisis, Trousseaus or Chvosteks sign Assess changes in voice pattern & for laryngeal nerve damage Administer calcium & vitamin D supplements as prescribed.

Parathyroid Hormones
Parathyroid hormone regulates serum calcium levels Low serum calcium level stimulate parathyroid hormone release Hyperparathyroidismgiven antihypercalcemics Hypoparathyroidismgiven calcium & Vit. D

CALCIUM SUPPLEMENTS
o o o calcium carbonate (Tums) calcium gluconate calcium lactate

VITAMIN D SUPPLEMENTS
o calcifediol (Calderol)

CALCIUM REGULATORS
o calcitonin human (Cibacalcin)

ANTIHYPERCALCEMICS
o edetate disodium (Disotate)

Hyperparathyroidism
Primary hyperparathyroidism
Causes hypercalcemia and increase calcium in the urine filtrate leading to hypercalciuria --> kidney stones Chronic bone resorption may produce demineralization, pathologic fractures, and cystic bone lesion. Involves hyperplasia of the glands Occurs primarily in persons with renal failure

Secondary hyperparathyroidism

Assessment Clinical Manifestation: hypercalcemia & hypophosphatemia, fatigue & muscle weakness, skeletal pain & tenderness, bone deformities resulting from pathologic fractures, weight loss, constipation, hypertension, cardiac dysrhythmias

You might also like