powerpoint endocrine

MANAGEMENTS OF PATIENTS WITH ALTERATIONS IN

METABOLISM

ANATOMY AND PHYSIOLOGY

PITUITARY GLAND

THYROID GLAND

Pituitary Gland Disorders

Anterior Pituitary Gland Disorders

Hormone Increased level Decreased level

GH Gigantism (child)

Acromegaly (adult)

Dwarfism (child)

Lethargy, premature aging

ACTH Cushing’s Disease Addison’s Disease

TSH Goiter, increased BMR, HR, BP

Graves disease

Decreased BMR, HR, CO, BP

Cretinism (children)

Prolactin amenorrhea Too little milk

FSH Late puberty, infertility

LH Menstrual cycle disturbance

Amenorrhea, impotence

Posterior Pituitary Gland Disorders

Hormone Increased Decreased

Oxytocin Precipitates childbirth, excess milk

Prolonged childbirth, diminished milk

ADH (vassopressin)

Increased BP, decreased urinary output, edema.

SIADH

Diabetes insipidus, dilute urine & increased urine output

Anterior Pituitary Gland Disorders

GROWTH HORMONE EXCESS

Gigantism

– An excessive secretion of growth hormones in children.

– May grow as tall as 8 feet (240cm) and weigh more than 300 lbs. (136 kg).

Gigantism

GROWTH HORMONE EXCESS

Acromegaly

• An excessive secretion of growth hormones in adults.

• Characterized by an overgrowth of the bones and soft tissue.

• Bones increase in thickness and width.

Acromegaly

Symptoms:• Enlarged hands & feet• Fingertips tufted or clubbed like appearance• Mild joint pain to deforming, crippling arthritis• Coarsening of facial features• Sleep apnea• General tiredness• Vision disturbance• Headaches• Polydipsia• Polyuria

Acromegaly

Diagnostic Studies

• History taking• Physical examination• Evaluation of IGF-1 levels, IGF binding protein-3

(IGFBP-3) levels• GH response to oral glucose challenge test – definitive

diagnosis• MRI, CT scan, ophthalmic examinatioin – is indicated

for identifying tumor and determining the extent of spread of the pituitary tumor into surrounding tissue.

Surgical Management

Hypophysectomy

Radiation Therapy

• Radiation therapy is considered when surgery has failed to produce complete remission.

• Because of the length of time it takes to achieve GH reduction, radiation therapy is usually offered in combination with drugs that reduce GH levels.

• Radiation has also been used to reduce the size of the tumor before surgery.

Pharmacologic Management

• Somatostatin analogs• Octreotide is the most common drug used

for acromegaly. It is a somatostatin analog that reduces GH levels to within the normal range in many patients. Octreotide is given by subcutaneous injection three times a week.


• GH receptor antagonist• Pegvisomant is a GH receptor antagonist and is

considered an alternative to somastostatin analogs. This drug is used for patients who have received surgery or radiation therapy, but still have hypersecretion of GH. It is not considered appropriate for primary treatment because this agent only blocks hormone action rather than acting on the tumor itself.

•


• Dopamine agonist• May also be used in treatment of

acromegaly to supress GH secretion. Dopamine agonist may be tried first because they are less expensive than the other two classes of drugs, but they are often not effective.

Nursing Management

• Patient should be instructed to avoid vigorous coughing, sneezing and straining at stool to prevent cerebrospinal fluid leakage from the point at which the sella turcica was entered.

• Head of the patient’s bed should be elevated at a 30 degree angle at all times. This elevation avoids pressure on the sella turcica and decreases headaches, a frequent

postoperative problem.

Nursing Management

• Monitor neurologic status including pupillary response, should be done in order to detect neurologic complications.

• Any clear nasal drainage should be sent to the laboratory to be tested for glucose.

Nursing Management

• Mild analgesia is given for headaches.

• The nurse should perform mouth care every 4 hours to keep surgical area clean and free from debris and to promote patient comfort.

• Toothbrushing should be avoided for atleast 10 days to prevent disrupting the suture line and to avoid discomfort.

DWARFISM

• Dwarfism is short stature that results from a genetic or medical condition.

DWARFISM

• Dwarfism is generally defined as an adult height of 4 feet 10 inches or less (147 centimeters). The average adult height among people with dwarfism is 4 feet (122 cm).

Types

• Disproportionate dwarfism. If body size is disproportionate, some parts of the body are small, and others are of average size or above-average size.

• Proportionate dwarfism. A body is proportionately small if all parts of the body are small to the same degree and appear to be proportioned like a body of average stature.

Causes

• Achondroplasia

• Turner syndrome

• Growth hormone deficiency

Clinical Manifestations

The most common cause of dwarfism is a disorder called achondroplasia, which causes disproportionately short stature. This disorder usually results in the following:•An average-size trunk •Short arms and legs, with particularly short upper arms and upper legs •Short fingers, often with a wide separation between the middle and ring fingers


• Limited mobility at the elbows • A disproportionately large head, with a

prominent forehead and a flattened bridge of the nose

• Progressive development of bowed legs (genu varum)

• Progressive development of swayed lower back (lordosis)

• An adult height around 4 feet — about 122 cm


Another cause of disproportionate dwarfism is a rare disorder called spondyloepiphyseal dysplasia congenita (SEDC). Signs may include: •A very short trunk, which may or may not be apparent in infancy •A short neck •Shortened arms and legs •Average-size hands and feet •Slightly flattened cheekbones


• Hip deformities that result in thighbones turning inward (coxa vara)

• A foot that's twisted or out of shape (clubfoot) • Progressive hunching curvature of the upper

spine (kyphosis) • Progressive development of lordosis • Vision and hearing problems • Adult height ranging from 3 feet (91 cm) to just

over 4 feet (122 cm)


Growth hormone deficiency is a relatively common cause of proportionate dwarfism. It occurs when the pituitary gland fails to produce an adequate supply of growth hormone, which is essential for regular childhood growth. Signs include: •Height below the third percentile on standard pediatric growth charts •Growth rate slower than expected for age •Delayed or no sexual development during adolescence

Tests and Diagnosis

• Measurements

• Appearance

• Imaging

• Genetic tests

• Family history

• Hormone tests

Common surgical treatments

Surgical procedures that may correct problems with bones in people with disproportionate dwarfism include:

• Inserting metal staples into the ends of long bones where growth occurs (growth plates) in order to correct the direction in which bones are growing

• Dividing a limb bone, straightening it and inserting metal plates to hold it in place

Common surgical treatments

• Inserting rods or staples to help correct the shape of the spine

• Increasing the size of the opening in bones of the spine (vertebrae) to alleviate pressure on the spinal cord

Management

• Limb lengthening

• Hormone therapy

Lifestyle and home remedies

• Car seats

• Infant carriers and play equipment

• Adequate support

• Complications

• Posture

• Healthy diet

• Healthy activities

Posterior Pituitary Gland Disorders

SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE

• SIADH occurs when ADH is released despite normal or low plasma osmolarity.

• SIADH results from an abnormal production or sustained secretion of adh and is characterized by fluid retention, serum hypoosmolality, dilutional hyponatremia, hypochloremia, concentrated urine in the presence of normal or increased intravascular volume and normal renal function.

Clinical Manifestaions

• muscle cramps and weakness• thirst, dyspnea on exertion, fatigue and dulled

sensorium • low urinary output and increased body weight. • severe and include vomiting, abdominal cramps,

muscle twitching, and seizures• cerebral edema may occur, leading to lethargy,

anorexia, confusion, headache, seizures and coma.

Diagnostic Studies

• The diagnosis of SIADH is made by simultaneous measurements of urine and serum osmolality. The dilutionla hyponatremia is indicated by a serum sodium less than 134mEq/L, serum osmolality less than 280 mOsm/kg and urine specific gravity greater than 1.005. A serum osmolality much lower than the urine osmolality indicates the inappropriate excretion of concentrated urine in the presence of dilute serum.

Management

• Once SIADH is diagnosed, treatment is directed at the underlying cause.

• Medications that stimulate the release of ADH should be avoided or discontinued.

• IV hypertonic saline solution may be administered in cases of severe hyponatremia especially in the presence of neurologic symptoms such as seizures,.

Management

• Hypertonic saline requires a very slow infusion rate on an infusion pump to avoid too-rapid a rise in sodium.

• A diuretic such as furosemide (lasix) may be used to promote diuresis, but only if the serum sodium is at least 125 mEq/L, because it may promote further loss of sodium. Because furosemide increases potassium, calcium and magnesium losses, supplements may be needed.

Management

• Fluid restriction of 500 ml per day is also indicated for those with severe hyponatremia.

• In chronic SIADH, water restriction of 800-1000 ml per day is recommended. Because this degree of restriction may not be tolerated, demeclocycline (declomycin) and lithium may be administered. These agents block the effect of ADH on the renal tubules, thereby allowing a more dilute urine.

Nursing Management

• Restrict total fluid intake to no more than 1000ml/day (including that taken with medications)

• Position head of the bed flat or with no more than 10 degrees of elevation to enhance venous return to heart and increase left atrial filling pressure, reducing ADH release

• Protect from injury (eg. Assist with ambulation, bed arm) because of potential alterations in mental status.

Nursing Management

• Seizure precautions• Frequent turning, positioning and ROM exercise

(if patient is bed ridden).• Frequent oral hygiene• Provide distractions to decrease the discomfort of

thirst related to fluid restrictions.• Provide support for patient significant others

regarding diagnosis and many mental status changes.

DIABETES INSIPIDUS

• Diabetes insipidus is associated with a deficiency of production or secretion of ADH or a decreased renal response to ADH. Decrease in ADH results in fluid and electrolyte imbalances caused by increased urinary output and increased plasma osmolality.

Classification

TYPES CAUSES

Central DI (neurogenic)

Problem results from an interference with ADH synthesis or release. Multiple causes include brain tumor, head injury, brain surgery, CNS infections

Nephrogenic DI

Problems results from inadequate renal response to ADH despite presence of adequate ADH. Caused by drug therapy, renal damage or hereditary renal disease

Psychogenic DIProblem results from excessive water intake. Caused by structural lesion in thirst center or psychologic disorder


• increased thirst (polydypsia) and increased urination (polyuria)

• fatigued from nocturia

• generalized weakness

• Central DI - excessive fluid loss,triphasic pattern: the acute phase, interphase, and third phase


• weight loss, constipation, poor tissue turgor, hypotension, tachycardia and shock.

• irritability and mental dullness to coma.

• severe dehydration and hypovolemic shock

Diagnostic Studies

• Complete history taking

• Physical assessment

• Water deprivation test

Management

• Hypotonic saline or dextrose 5% in water is administered intravenously and titrated to replace urinary output

• Hormone replacement

• Desmopressin acetate (DDAVP)

Management

• Aqueous vasopressin (pitressin), vasopressin tannate and lysine vasopressin (diapid)

• Chlorpropamide (diabinese) and carbamazepine (tegretol)

• dietary measures (low-sodium diet) and thiazide diuretics

• indomethacin (indocin)

Nursing Management

• administer fluids and hormone replacement

• Adequate fluids should be kept at the bedside

• Accurate records of intake and output, urine specific gravity and daily weights are mandatory in the assessment of fluid volume status.

Nursing Management

• Administration of DDAVP.

• Assesss for weight gain, headache, restlessness, and signs of hyponatremia and water intoxication

• The patient with chronic DI who requires long term ADH replacement needs instruction in self-mangement.

Nursing Management

• DDAVP can be taken orally or intransally. • Headache, nausea, and other signs of

hyponatremia may indicate overdosage. • Failure to improve may indicate underdosage. • Patients taking DDAVP should be instructed to

monitor their daily weight. • Increase in daily weight may indicate fluid

retention.

DISORDERS OF THE THYROID GLAND

GOITER

• Hypetrophy and enlargement of the thyroid gland caused by excess TSH stimulation, which in turn can be caused by inadequate circulating thyroid hormone


• A visible swelling at the base of your neck that may be particularly obvious when you shave or put on makeup

• A tight feeling in your throat• Coughing• Hoarseness• Difficulty swallowing• Difficulty breathing

Etiology

• Iodine deficiency• Graves' disease• Hashimoto's disease• Multinodular goiter• Solitary thyroid nodules• Thyroid cancer• Pregnancy• Inflammation

Tests and diagnosis

• Hormone test

• Antibody test

• Ultrasonography

• Thyroid scan

• Biopsy

Treatments and Drugs

• Observation.

• Medications:levothyroxine (Levothroid, Synthroid)

• Surgery

• Radioactive iodine

Lifestyle and home remedies

• Get enough iodine

• Reduce iodine consumption

THYROID NODULES

A thyroid nodule, a palpable deformity of the thyroid gland, may be benign or malignant. Benign nodules are usually not dangerous, but they can cause tracheal compression if they become too large. Malignant tumors of the thyroid gland are not common. The major sign of thyroid cancer is the presence of a hard, painless nodule or nodules on an enlarged thyroid gland.

Diagnostic Exam

• Ultrasound

• Computed tomography

• MRI

• Ultrasound-guided fine-needle aspiration

• Thyroid scan

Surgical Management

• Unilateral total lobectomy with removal of the isthmus

• total thyroidectomy with bilateral lobectomy

Nursing Management

• Nursing care for the patient with thyroid tumors is similar to care for the patient who has undergone thyroidectomy and also includes general nursing measures for the patient with cancer.

THYROIDITIS

• Thyroiditis is an inflammatory process in the thyroid that can have several causes.

• Subacute granulomatous thyroiditis (de Quervain’s thyroiditis), which causes thyrotoxicosis, is thought to be caused by a viral infection.

THYROIDITIS

• Acute thyroiditis is due to bacterial or fungal infection

• Chronic autoimmune thyroiditis Hashimoto’s thyroiditis is a chronic autoimmune disease in which thyroid tissue is replaced by lymphocytes and fibrous tissue.It can lead to hypothyroidism.

•

THYROIDITIS

• Silent painless thyroiditis is form of lymphocytic thyroiditis with a variable onset. In women, this condition may occur in the post partum period and usually resolves within 3 to 12 months.It is believed to be an autoimmune disease and may be early Hashimoto’s thyroiditis.

Management

• Recovery from thyroiditis may be complete in weeks or months without treatment.

• If the condition is bacterial in origin, treatment may include specific antibiotics or surgical drainage.

• In the subacute and acute forms, salicylates and nonsteroidal anti-inflammatory drugs are used.

Management

• If there is no response to these drugs in 50 hours, corticosteroids are given.

• Propanolol or atenolol may be used for cardiovascular symptoms from a hyperthyroid condition.

• Thyroid hormone replacement is indicated if the patient is hypothyroid.

Nursing Management

• Education regarding treatment and encouraging compliance are important for all types of thyroiditis.

• Patient should be instructed to remain under close health care supervision so that progress can be monitored and to report any change in symptoms to the health care provider.

HYPERTHYROIDISM

• Hyperthyroidism is hyperactivity of the thyroid gland with sustained increase in synthesis and release of thyroid hormones. The term thyrotoxicosis refers to the physiologic effects or clinical syndrome of hypermetabolism that result from exess circulating levels of T4 , T3 or both.

Etiology and Pathophysiology

• Grave’s Disease is an autoimmune disease of unknown etiology marked by diffused thyroid enlargement and excessive thyroid hormone secretion. Precipitating factors such as insufficient iodine supply, infection and stressful life events may interact with genetic factors to cause Grave’s disease.

• Toxic Nodular Goiters. Nodular goiters are thyroid hormone secreting nodules that function independent of TSH stimulation. If these nodules are associated with hyperthyroidism, they are termned toxic.


• Palpation of the thyroid may reveal goiter.

• Auscultation of the thyroid may reveal bruits

• Upper lids are usually retracted and elevated

• Sclera visible above the iris.

• Corneal ulcers and eventual loss of vision,


• Opthalmopathy• Exophthalmos

Complications

• Thyrotoxic crisis also called thyroid storm is an acute, rare, condition in which all hyperthyroid manifestations are heightened.

• Although it is considered a life threatening emergency, death is rare when treatment is vigorous and initiated early.

Thyrotoxic crisis

• The physiologic factor is unknown.

• The cause is thought to be stressors in a patient with preexisting hyperthyroidism, either diagnosed or undiagnosed.

• Heart and nerve tissues become more sensitive to catecholamines due to more binding sites for epinephrine and norepinephrine.

Thyrotoxic crisis

• Manifestations include severe tachycardia, heart failure, shock, hyperthermia (up to 105.3 F or 40.7 c), restlessness, agitation, seizure, abdominal pain, nausea, vomiting, diarrhea, delirium, and coma.

• Treatment is aimed at reducing circulating thyroid hormone levels and the clinical manifestations of this disorder by appropriate drug therapy.

Thyrotoxic crisis

• Supportive therapy is directed at managing respiratory distress, fever reduction, fluid replacement and elimination or management of the initiating stressors.

Diagnostic Studies

• History and physical examination

• Ophthalmic examination

• ECG

• Radioactive Iodine Uptake (RAIU)

• Laboratory test– Serum Free T4, TSH levels– TRH stimulation test


• Antithyroid Drugs– Propythiouracil (PTU)– Mathimazole (Tapazole)

• Iodine

• B-adrenergic Blockers

Radioactive Therapy

• Radioactive iodine (RAI) therapy is the treatment of choice for most nonpregnant adults. RAI damages or destroys thyroid tissue, thus limiting thyroid hormone secretion.

Surgical Management

• Thyroidectomy

• Endoscopic thyroidectomy

Nursing Mangement

• A calm and quiet room should be provided because increased metabolism causes sleep disturbances.

• If exophthalmos is present, there is potential for corneal injury related to irritation and dryness.

• Nursing interventions to relieve eye discomfort and prevent corneal ulceration include applying artificial tears to soothe and moisten membranes.

Nursing Mangement

• Salt restriction may help reduce periorbital edema.

• Elevation of patient’s head promotes fluid drainage from periorbital area; the patient should sit upright as much as possible.

• Dark glasses reduce glare and prevent irritation from smoke, air currents, dust and dirt.

Nursing Mangement

After thyroidectomy the nurse should do the following:•Assess the patient every 2 hours for 24 hours for signs of hemorrhage or tracheal compression such as irregular breathing, neck swelling, frequent swallowing, sensations of fullness at incision site, choking and blood on the anterior or posterior dressings.

Nursing Mangement

• Place the patient in a semi fowler position and support the patient’s head with pillows and avoid flexion of the neck and any tension on the suture lines.

Nursing Mangement

• Monitor vital signs. Complete the initial assessment by checking for signs of tetany secondary to hypoparathyroidism and by evaluating difficulty speaking and hoarseness. Trousseau’s sign and Chvostek’s sign should be monitored for 72 hours. Some hoarseness is to be expected for 3 to 4 days after surgery because of edema.

HYPOTHYROIDISM

• Hypothyroidism results from insufficient circulating thyroid hormone as a result of a variety of abnormalities.

• Hypothyroidism can be primary (related to destruction of thyroid tissue or defective hormone synthesis) or secondary (related to pituitary disease with decreased THS secretion or hypothalamic dysfunction with decreased thyrotropin-releasing hormone [TRH] secretion)..

HYPOTHYROIDISM

• It may also be transient, related to thyroiditis or discontinuance of thyroid hormone therapy.

• Iodine deficiency is the most common cause of hypothyroidism worldwide and is most prevalent in iodine-deficient areas of the world.

HYPOTHYROIDISM

• Hypothyroidism that develops in infancy (termed cretinism) is caused by thyroid hormone deficiencies during fetal or early neonatal life.


• Fatigued and lethargic, and experiences personality and mental changes

• Mental changes - impaired memory, slowed speech, decreased initiative, somnolence and may appear depressed

• low exercises tolerance and shortness of breath on exertion


• Anemia

• bruise easily

• Increased serum cholesterol and triglyceride levels and the accumulation of mucopolysaccharides in the intima of small blood vessels

• GI motility is also decreased in hypothyroidism, and achlorhydria (absence or decrease of hydrochloric acid)


• Constipation

• cold intolerance, hair loss, dry and coarse skin, brittle nails, hoarseness, muscle weakness and swelling, and weight gain.

• Weight gain


• Myxedema, the accumulation of hydrophilic mucopolysaccharides in the dermis and other tissues. This mucinous edema causes the characteristics facies of hypothyroidism (i.e., puffiness, periorbital edema, and masklike affect).

Complications

Myxedema coma can be precipitated by infection, drugs (especially opioids, tranquilizers, and barbiturates), exposure to cold, and trauma. It is characterized by subnormal temperature, hypotension, and hypoventilation.

Diagnostic Studies

• history and physical examination

• Serum TSH levels

• Other abnormal laboratory findings are elevated cholesterol and triglycerides, anemia, and increased creatine kinase.

Collaborative Care

• A low-calorie diet is indicated to promote weight loss.

• Levothyroxine (Synthroid)

• Liotrix

Nursing Management

Nursing Assessment

• Assessment of the patient who is suspected of having hypothyroidism should include questions about weight gain, mental changes, fatigue, slowed and slurred speech, cold in tolerance, skin changes such as increased dryness or thickening, constipation and dyspnea.

Nursing Management

• In addition, the nurse should question the patient about the recent introduction of iodine-containing medications. The patient should be assessed for bradycardia; distended abdomen; dry, thick, cold skin; thick, brittle nails; parethesias; and muscular aches and pains.

Nursing Management

Acute Intervention

• Patient who develops myxedema coma requires acute nursing care, often in an intensive care setting. Mechanical respiratory support and cardiac monitoring are frequently necessary.

Nursing Management

• The nurse will administer thyroid hormone replacement therapy and all other medications IV because the paralytic ileus associated with myxedema coma causes unreliable absorption of oral medications.

• If the patient is hyponatremic, hypertonic saline may be administered until the serum sodium reaches at least 130 mEq/L (130 mmo1/L).

Nursing Management

• The nurse should monitor core temperature because the patient with myxedema coma is often hypothermic.

• For assessment of the patient’s progress, vital signs, body weight, fluid intake and output, and visible edema should be monitored. steadily to normal levels.

Nursing Management

Ambulatory and Home Care.

• Provide written instructions, repeat the information often, and assess the patient’s comprehensive level.

• The need for lifelong drug therapy must be stressed..

Nursing Management

• The patient must be taught to contact a health care provider immediately if signs of overdose appear, such as orthopnea, dyspnea, rapid pulse, palpitations, nervousness, or insomnia.

• The patient with diabetes, mellitus should test his or her capillary blood glucose at least daily because return to the euthyroid state frequently increases insulin requirements.

DISORDERS OF THE PARATHYROID GLAND

HYPERPARATHYROIDISM

• Hyperparathyroidism is a condition

involving an increased secretion of parathyroid hormone (PTH).

PARATHYROID GLAND

Primary hyperparathyroidism

• due to an increased secretion of PTH leading to disorders of calcium, phosphate, and bone metabolism

• Common cause is a benign tumor (adenoma) in the parathyroid gland

• occurs between 30 to 70 years of age and peak incidence is in the 40s and 50s

• Patients who have previously undergone head and neck radiation may have an increased risk of developing a parathyroid adenoma.

Secondary hyperparathyroidism

• appears to be a compensatory response to conditions that induce hypocalcemia, the main stimulus of PTH secretion

• vitamin D deficiencies, malabsorption, chronic renal failure, and hyperphosphatemia.

Tertiary hyperparathyroidism

• occurs when there is hyperplasia of the parathyroid glands and a loss of negative feedback from circulating calcium levels. Thus there is autonomous secretion of PTH, even with normal calcium levels.


• Excessive levels of circulating PTH usually lead to hypercalcemia and hypophosphatemia

• In the bone density, cyst formation, and general weakness can occur as a result of the effect of PTH on osteoclastic (bone resorption) and osteoblastic (bone formation) activity


• In the kidneys, the excess calcium cannot be reabsorbed, leading to increased levels of calcium in the urine (hypercalciuria).

• This urinary calcium, along with a large amount of urinary phosphate, can lead to calculi formation


• PTH stimulates the syntheses of a biologically active form of vitamin D, a potent stimulator of calcium transport in the intestine. In this way, PTH indirectly increases GI absorption of calcium, which further contributes s to the high serum calcium levels.


• The major manifestations include weakness, loss of appetite, constipation, increased need for sleep, emotional disorders, and shortened attention span.

• Major signs include loss of calcium bones (osteoprosis), fractures, and kidney stones (nephrolithiasis).


• Neuromuscular abnormalities are characterized by muscle weakness, particularly in the proximal muscles of the lower extremities.

Complications

• Serious complications of hyperparathyroidism are renal failure; pancreatitis; cardiac changes; and long bone, rib, and vertebral fractures.

Diagnostic studies

• PTH Serum levels

• Serum phosphorus level

• Elevations in other laboratory tests include urine calcium serum chloride, uric acid, creatinine, amylase (if pancreatitis is present), and alkaline phosphatase (in the presence of bone disease).

Diagnostic studies

• Bone density measurements, may also be used to detect bone loss. Conversely, individuals found to have bone loss on a screening dual-energy x-ray absorptiometry (DEXA) scan should be tested for hypercalcemia.

• MRI, CT, and/or ultrasound may be used for localization of the adenoma.

Surgical Therapy

• Parathyroidectomy

• Surgery involves partial or complete removal of the parathyroid glands.

• The most commonly used procedure involves an endoscope and is done on an outpatient basis

Surgical Therapy

• Autotransplantation of normal parathyroid tissue in the forearm or near the sternocleidomastoid muscle is usually done. This allows PTH secretion to continue with normalization of calcium levels. If autotransplantation is not possible, or if it fails, the patient will need to take calcium supplements for life.

Nonsurgical Therapy

• Annual examination with tests for serum PTH, calcium, phosphorus, and alkaline phosphatase levels; renal function; x-rays to sses for metabolic bone loss; and measurement of urinary calcium excretion.

• Continued ambulation and the avoidance of immobility

Nonsurgical Therapy

• Dietary measures also include maintenance of a high fluid intake and a moderate calcium intake.

• Phosphorus is usually supplemented unless contraindicated by an increased risk for urinary calculi formation.

Nonsurgical Therapy

• Bisphosphonates

• Estrogen or progestin therapy can reduce serum and urinary calcium levels in the postmenopausal woman and may retard demineralization of the skeleton.

• Oral phosphate may be used to inhibit the calcium-absorbing effects of vitamin D in the intestine.

Nonsurgical Therapy

• Diuretics may be given to increase the urinary excretion of calcium.

• Calcimimetic agents (e.g., cinacalcet [Sensipar]) are a new class of drugs that increase the sensitivity of the calcium receptor on the parathyroid gland, resulting in decreased PTH secretion and calcium blood levels, thus sparing calcium stores in the bone.

Nursing Management

• Nursing care for the patient following a parathyroidectomy is similar to that for a patient after thyroidectomy.

• The major postoperative complications are associated with hemorrhage and fluid and electrolyte disturbances.

Nursing Management

• Tetany, a condition of neuromuscular hyperexcitability associated with sudden decrease in calcium levels, is another concern.

• It is usually apparent early in the postoperative period but may develop over several days. gluconate or gluceptate should be readily available for patients following parathyroidectomy in the event that acute tetany occurs.

Nursing Management

• Mild tetany, characterized by unpleasant tingling of the hands and around the mouth, may be present but should decrease over time.

• If tetany becomes more severe (e.g., muscular spasms or laryngospasms develop), IV calcium may be given. IV calcium

Nursing Management

• Intake and output are monitored to evaluate fluid status.

• Calcium, potassium, phosphate, and magnesium levels are assessed frequently, as well as Chvostek’s and Trousseau’s signs.

• Mobility is encourage to promote bone calcification.

Nursing Management

• Assist the patient with hyperparathyroidism to adapt the meal plan to his or her life-style.

• Stress to the patient the importance of an exercise program. The patient should be encourage to keep the regular appointments, and the test being performed should be explained.

Nursing Management

• The patient should also be instructed in the symptoms of hypocalcemia or hypercalcemia and to report these should they occur.

HYPOPARATHYROIDISM

• Hypoparathyroidism, is a condition associated with inadequate circulating PTH, is uncommon.

• It is characterized by hypocalcemia resulting from lack of PTH to maintain serum calcium level may also occur (psuedohypoparathyroidism).

HYPOPARATHYROIDISM

• This is caused by a generic defect resulting in hypocalcemia in spite of normal of high PTH levels and is often associated with hypothyroidism and hypogonadism.

HYPOPARATHYROIDISM

• The most common cause of hyporarathyroidism is iatrogenic.

• This may include accidental removal of the parathyroid glands or damage to the vascular supply of the glands during neck surgery (e.g., thyroidectomy, radical neck surgery).

HYPOPARATHYROIDISM

• Idiopathic hypoparathyroidism resulting from the absence, fatty replacement, or atrophy of the gland is a rare disease that usually occurs early in life and may be associated with other endocrine disorders.

• Affected patients may have antiparathyroid antibodies.

• Severe hypomagnesemia also leads to a suppression of PTH secretion.


• The clinical features of acute hypoparathyroidism are due to hypocalcemia.

• Sudden decrease in calcium concentration causes tetany.

• This state is characterized by tingling of the lips, fingertips, and occasionally feet and increased muscle tension leading to paresthesia and stiffness.


• Painful tonic spasms of smooth and skeletal muscles, dysphagia, a constricted feeling in the throat, and layngospasms are also present.

• Chvostek’s sign and Trousseau’s sign are usually positive.

• Patients are usually anxious and apprehensive.


• Abnormal laboratory findings include decreased serum calcium and PTH levels and increased serum phosphate levels.

• Other causes of chronic hypocalcemia include chronic kidney disease, vitamin D deficiency and hypomagnesemia.

Nursing and Collaborative Care

• The primary management objectives for a patient with hypoparathyroidism are to treat acute complications such as tetany, maintain normal serum calcium levels, and prevent long-term complications.

• Emergency treatment of tetany requires the administration of IV calcium.


• IV calcium chloride, calcium gluconate, or calcium gluceptate should be given slowly.

• Calcium must be infused slowly because the high blood levels can cause hypotension, serious cardiac dysrhythmias, or cardiac arrest.


• IV calcium can cause venous irritation and inflammation. Extravasation may cause cellulitis, necrosis, and tissue sloughing.

• IV patency should be assessed before administration.


• Rebreathing may partially alleviate acute neuromuscular symptoms associated with hypocalcemia such as generalized muscle cramps or mild tetany.

• The patient who can cooperate should be instructed to breathe in and out of a paper bag or breathing mask.


• Oral calcium supplements of at least 1.5 to 3g/day is divided doses are usually prescribed.

• Vitamin D is used in chronic and resistant hypocalcemia to enhance intestinal calcium absorption and bone resorption.

• The patient should be instructed about the need for lifelong treatment and follow-up care including the monitoring of calcium levels three to four times a year.

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