Drug for Endocrine

Disease
 Diabetes Insipidus
 Deficiency of ADH
 Excessive thirst, large volumes of dilute urine
 Can occur secondary to brain tumors, head trauma,
infections of the CNS, and surgical ablation or radiation
 Nephrogenic DI—relates to failure of the renal tubules to
respond to ADH. Can be related to hypokalemia,
hypercalcemia and to medications (lithium demeocycline)
 Excessive thirst
 Urinary sp. gr. of 1.001.1.005
Assessment and Diagnostic Findings

 Fluid deprivation test—withhold fluids for 8-12

hours. Weigh patient frequently. Inability to slow
down the urinary output and fail to concentrate
urine are diagnostic. Stop test if patient is
tachycardic or hypotensive
 Trial of desmopressin and IV hypertonic saline
 Monitor serum and urine osmolality and ADH
levels
 Pharmacologic Tx and Nursing
Management

 Can also use Diabenese and thiazide diuretics in

mild disease as they potentiate the action of ADH
 Ifrenal in origin—thiazide diuretics, NSAIDs
(prostaglandin inhibition) and salt depletion may
help
 Educate patient about actions of medications, how
to administer meds, wear medic alert bracelet
 SIADH
Excessive ADH secretion
Retain fluids and develop a dilutional hyponatremia
Often non-endocrine in origin—such as bronchogenic carcinoma
Causes: Disorders of the CNS like head injury, brain surgery,
tumors, infections or medications like vincristine,
phenothiazines, TCAs or thiazide diuretics
Meds can either affect the pituitary or increase sensitivity to
renal tubules to ADH
Management: eliminate cause, give diuretics, fluid restriction,
lab chemistries
Restoration of electrolytes must be gradual
May use 3% NaCl in conjunction with Furosemide
 Thyroid
 Inspect gland
 Observe for goiter
 Check TSH, serum T3 and T4
 T3 resin uptake test useful in evaluating thyroid hormone levels
in patients who have received diagnostic or therapeutic dose of
iodine. Estrogens, Dilantin, Tagamet, Heparin, amiodarone,
PTU,steroids and Lithium can cloud the accuracy
 T3 more accurate indicator of hyperthyroidism according to text
 Thyroid
 Antibodies
seen in Hashimoto’s, Grave’s and other auto-
immune problems.
 Radioactive iodine uptake test measures rate of iodine
uptake. Patients with hyperthyroidism exhibit a high uptake,
hypothyroidism will have low uptake
 Thyroid scan—helps determine the location, size, shape and
size of gland. “Hot” areas (increased function) and “cold”
areas (decreased function) can assist in diagnosis.
 Hypothyroidism
Most common cause is Hashimoto’s thyroiditis
Common in those previously treated for hyperthyroidism
Atrophy of gland with aging
Medications like lithium, iodine compounds, antithyroid
meds can cause
Radiation treatments to head and neck
Infiltrative diseases like amyloidosis, scleroderma
Iodine deficiency and excess
Hypothalamic or pituitary abnormality
 Pharmacologic Management of
hypothyroidism
 Levothyroxine is preferred agent
 Dosage is based on TSH
 Desiccated thyroid used infrequently due to inconsistent
dosing
 Angina
can occur when thyroid replacement is initiated as it
enhances effects of cardiovascular catecholamines (in pt.
w/pre-existent CAD). Start at low dose.
 Hypnotics and sedatives may have profound effects on
sensorium
 Hyperthyroidism

Extreme form is Grave’s disease

Caused by thyroiditis, excessive
amount thyroid hormone, abnormal
output by immunoglobulins
Is more common in women
 Manifestations of hyperthyroidism

 Thyrotoxicosis—nervousness, irritable,
apprehensive, palpitations, heat intolerance, skin
flushing, tremors, possibly exophthalmos
 Have an increased sensitivity to catecholamines
 Can occur after irradiation or presence of a tumor
 Management

 Reduce thyroid hyperactivity—usually use

radioactive iodine, antithyroid meds or
surgery)
 Beta blockers
 Can be relapse with antithyroid medication
 Pharmacologic Therapy
Irradiation with administration of radioisotope iodine 131—
initially may cause an acute release of thyroid hormones. Should
monitor for thyroid storm
S/S of thyroid storm—high fever. Tachycardia, delirium, chest
pain, dyspnea, palpitations, weight loss, diarrhea, abdominal pain
Management of thyroid storm—oxygen, IV fluids with dextrose,
hypothermic measures, steroids to treat shock or adrenal
deficiency, iodine to decrease output of T4, beta blockers, PTU or
Tapazole impedes formation of thyroid hormone and blocks
conversion of T4 to T3
 Antithyroid Medications
 PTU—propylthiouracil—blocks synthesis of hormones
 Tapazole (methimazole)—blocks synthesis of hormones.
More toxic than PTU.
 Sodium Iodide-suppresses release of thyroid hormone
 SSKI (saturated solution of potassium chloride)– suppresses
release of hormones and decreases vascularity of thyroid.
Can stain teeth
 Dexamethazone—suppresses release of thyroid hormones
 Nursing Management
 Reassurance r/t the emotional reactions experienced
 May need eye care if has exophthalmos
 Maintain normal body temperature
 Adequate caloric intake
 Managing potential complications such as dysrhythmias and
tachycardias
 Educate about potential s/s of hypothyroidism following any
antithyroid tx.
 Parathyroid Glands
Parathormone maintains sufficient serum calcium levels
Excess calcium can bind with phosphate and precipitate in
various organs, can cause pancreatitis
Hyperparathyroidism will cause bone decalcification and
development of renal calculi
More common in women
Secondary hyperparathyroidism occurs in those with chronic
renal failure and renal rickets secondary to excess
phosphorus retention (and increased parathormone
secretion)
 Manifestations of Hyperparathyroidism
 May be asymptomatic
 Apathy, fatigue, muscle weakness, nausea,
vomiting, constipation, hypertension and cardiac
dysrhythmias
 Excess calcium in the brain can lead to psychoses
 Renal lithiasis can lead to renal damage and even
failure
 Demineralization of bones with back and joint
pain, pain on weight bearing, pathologic fractures
 Peptic ulcers and pancreatitis can also occur
 Assessment and Diagnostic Findings

 Persistent elevated calcium levels

 Elevated serum parathormone level
 Bone studies will reveal decreased density
 Double antibody parathyroid hormone test is used
to distinguish between primary
hyperparathyroidism and malignancy
 Ultrasound, MRI, thallium scan, fine needle biopsy
also can be used to localize cysts, adenomas, or
hyperplasia
 Management
 Recommended treatment for his surgical removal
 Hydration therapy necessary to prevent renal calculi
 Avoid thiazide diuretics as they decrease renal excretion
of calcium
 Increase mobility to promote bone retention of calcium
 Avoid restricted or excess calcium in the diet
 Fluids, prune juice and stool softeners to prevent
constipation
 Watch for s/s of tetany postsurgically (numbness,
tingling, carpopedal spasms) as well as cardiac
dysrhythmias and hypotension
 Hypoparathyroidismfollowing

 Seen most often removal of thyroid gland,

parathyroid glands or following radical neck
surgery
 Deficiencyof parathormone results in increased
bone phosphate and decreased blood calcium
levels
 In absence of parathormone, there is decreased
intestinal absorption of dietary calcium and
decreased resorption of calcium from bone and
through kidney tubules
 Assessment and Diagnostic Findings

 Trousseau’s sign—can check with a BP cuff

 Chvostek’s sign—tapping over facial nerve causes
spasm of the mouth, nose and eye
 Labstudies may reveal calcium levels of 5-6
mg/dL or lower
 Serum phosphate levels will be decreased
 Management of Hypoparathyroidism

 Restore calcium level to 9-10 mg/dL

 May need to give IV calcium gluconate for immediate
treatment
 Use of parathormone IV reserved for extreme situations
due to the probability of allergic reactions
 Monitor calcium levels
 May need bronchodilators and even ventilator assistance
 Diet high in calcium and low in phosphorus; thus, avoid
milk products, egg yolk and spinach.
Management of Hypoparathyroidism

 Keep calcium gluconate at bedside

 Ensure has IV access
 Cardiac monitoring
 Care of postoperative patients who have
undergone thyroid surgery, parathyroidectomy or
radical neck surgery. Be watchful for signs of
tetany, seizures, and respiratory difficulties
 Cushing’s Syndrome

 Results from excessive adrenocortical activity

 May be related to excessive use of corticosteroid
medications or due to hyperplasia of the adrenal
cortex
 Oversecretion of corticosteroids can also be
caused by pituitary tumor
 Manifestations of Cushing’s syndrome

 Cataracts, glaucoma
 Hypertension, heart failure
 Truncal obesity, moon face, buffalo hump, sodium
retention, hypokalemia, hyperglycemia, negative nitrogen
balance, altered calcium metabolism
 Decreased inflammatory responses, impaired wound
healing, increased susceptibility to infections
 Osteoporosis, compression fractures
 Peptic ulcers, pancreatitis
 Thinning of skin, striae, acne
 Mood alterations
 Medical Management
 If pituitary source, may warrant transphenoidal
hypophysectomy
 Radiation of pituitary also appropriate
 Adrenalectomy may be needed in case of adrenal
hypertrophy
 Temporary replacement therapy with hydrocortisone or
Florinef
 Adrenal enzyme reducers may be indicated if source if
ectopic and inoperable. Examples include: ketoconazole,
mitotane and metyrapone.
 If cause is r/t excessive steroid therapy, tapering slowly to
a minimum dosage may be appropriate.