Assessment and Management of

Patients with Endocrine Disorders
By Linda Self
Glands of the Endocrine System
Posterior Pituitary
Anterior Pituitary
Pancreatic islets
Ovaries and testes
Releasing and inhibiting hormones
Corticotropin-releasing hormone
Thyrotropin-releasing hormone
Growth hormone-releasing hormone
Gonadotropin-releasing hormone
Somatostatin-=-inhibits GH and TSH
Anterior Pituitary
Growth Hormone--
Adrenocorticotropic hormone
Thyroid stimulating hormone
Follicle stimulating hormone—ovary in female, sperm
in males
Luteinizing hormone—corpus luteum in females,
secretion of testosterone in males
Prolactin—prepares female breasts for lactation
Posterior Pituitary
Antidiuretic Hormone

Oxytocin—contraction of uterus, milk ejection from
Adrenal Cortex
Mineralocorticoid—aldosterone. Affects sodium
absorption, loss of potassium by kidney

Glucocorticoids—cortisol. Affects metabolism,
regulates blood sugar levels, affects growth, anti-
inflammatory action, decreases effects of stress

Adrenal androgens—dehydroepiandrosterone and
androstenedione. Converted to testosterone in the
Adrenal Medulla
Epinephrine and norepinephrine
serve as neurotransmitters for sympathetic system
Follicular cells—excretion of triiodothyronine (T3)
and thyroxine (T4)—Increase BMR, increase bone and
calcium turnover, increase response to catecholamines,
need for fetal G&D
Thyroid C cells—calcitonin. Lowers blood calcium
and phosphate levels
Parathyroid hormone—regulates serum calcium
Pancreatic Islet cells

Glucagon—stimulates glycogenolysis and

Somatostatin—decreases intestinal absorption of
1, 25 dihydroxyvitamin D—stimulates calcium
absorption from the intestine
Renin—activates the RAAS
Erythropoietin—Increases red blood cell production
Progesterone—inportant in menstrual cycle,*maintains
Androgens, testosterone—secondary sexual
characteristics, sperm production
Releases thymosin and thymopoietin
Affects maturation of T lymphocetes
Affects sleep, fertility and aging
Work locally
Released by plasma cells
Affect fertility, blood clotting, body temperature
Health history—energy level, hand and foot size
changes, headaches, urinary changes, heat and cold
intolerance, changes in sexual characteristics,
personality changes, others
Physical assessment—appearance including hair
distribution, fat distribution, quality of skin,
appearance of eyes, size of feet and hands, peripheral
edema, facial puffiness, vital signs
Diagnostic Evaluation
Serum levels of hormones
Detection of antibodies against certain hormones
Urinary tests to measure by-products (norepinephrine,
metanephrines, dopamine)
Stimulation tests—determine how an endocrine gland
responds to stimulating hormone. If the hormone
responds, then the problem lies w/hypothalmus or
Suppression tests—tests negative feedback systems
that control secretion of hormones from the
hypothalamus or pituitary.
Disorders of the Pituitary
Pituitary Tumors
Eosinophilic tumors may result in gigantism or in
acromegaly. May suffer from severe headaches, visual
disturbances, decalcification of the bone, endocrine
Basophilic tumors may cause Cushing’s syndrome
w/features of hyperadrenalism, truncal obesity,
amenorrhea, osteoporosis
Chromophobic tumors—90% of pituitary tumors.
Present with lowered BMR, obesity, somnolence, scant
hair, low body temp, headaches, visual changes
Growth hormone deficiency in childhood will result in
primary dwarfism.
Pituitary Tumors—Assessment and
Diagnostic Findings
Vision tests
Serum levels of pituitary hormones, others
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
Excessive thirst
Urinary sp. gr. of
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
Trial of desmopressin and IV hypertonic saline
Monitor serum and urine osmolality and ADH levels
Pharmacologic Tx and Nursing
DDAVP—intranasal bid
Can be given IM if necessary. Every 24-96h. Can
cause lipodystrophy.
Can also use Diabenese and thiazide diuretics in mild
disease as they potentiate the action of ADH
If renal 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
Excessive ADH secretion
Retain fluids and develop a dilutional hyponatremia
Often non-endocrine in origin—such as bronchogenic
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 (Lasix),
fluid restriction, I&O, daily wt., lab chemistries
Restoration of electrolytes must be gradual
May use 3% NaCl in conjunction with Lasix
T3 and T4
Need iodine for synthesis of hormones—excess will
result in adaptive decline in utilization called the Wolf-
Chaikoff mechanism
Thyroid is controlled by TSH
Cellular metabolism, brain development, normal
growth, affect every organ in the body
T3 is five times as potent as T4
Calcitonin—secreted in response to high levels of
serum calcium, increases deposition in the bone
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
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.
Nursing Implications
Be aware of meds patient is taking (see list in text) that
can affect accuracy of testing
Also be aware if patient is taking multivitamins and
food supplements
 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
 More common in women, especially over age 50
From mild symptoms to myxedema
Myxedema –accumulation of mucopolysaccharides in
sc and interstitial tissues. Is the extreme form of
hypothyroidism. Can progress to shock.
S/S—fatigue, hair loss, dry skin, brittle nails,
numbness and tingling of the fingers, amenorrhea,
weight gain, decreased heart rate and temperature,
lassitude, cognitive changes, elevated cholesterol
levels, constipation, hypotension
Pharmacologic Management of
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
Management in Myxedema
Cautious fluid replacement
Glucose to restore to normal glycemic levels
Avoid rapid overheating due to increased oxygen
demands but keep warm
May give levothyroxine intravenously
With recovery,
Modify activity
High fiber foods
Home health for follow-up
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
Assessment and Diagnosis
Thyroid thrill and or bruit may be present
Thyroid may be enlarged
Decreased TSH, increased free T4 and an increased
radioactive iodine uptake
Reduce thyroid hyperactivity—usually use radioactive
iodine, antithyroid meds or surgery)
Beta blockers
Can be relapse with antithyroid meds
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
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
Surgical Management
Reserved for special circumstances, e.g. large goiters,
those who cannot take antithyroid meds, or who need
rapid normalization
Subtotal thyroidectomy
Before surgery, give PTU until s/s of hyperthyroidism
have disappeared
Iodine may be used to decrease vascularity
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
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
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
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
Ultrasound, MRI, thallium scan, fine needle biopsy
also can be used to localize cysts, adenomas, or
 Recommended treatment for hyperparathyroidism is
surgical removal
 Hydration therapy necessary to prevent renal calculi
 Avoid thiazide diuretics as they decrease renal excretion of
 Increase mobility to promote bone retention of calcium
 Avoid restricted or excess calcium in the diet
 Fluids, prune juice and stool softeners to prevent
 Watch for s/s of tetany postsurgically (numbness, tingling,
carpopedal spasms) as well as cardiac dysrhythmias and
Hypercalcemic crisis
Seen with levels greater than 15mg/dL
Can result in life-threatening neurologic,
cardiovascular and renal symptoms
Treatments include: hydration, loop diuretics to
promote excretion of calcium, phosphate therapy to
promote calcium deposition in bone and reducing GI
absorption of calcium
Give calcitonin or mithramycin to decrease serum
calcium levels quickly
Seen most often following removal of thyroid gland,
parathyroid glands or following radical neck surgery
Deficiency of 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
Clinical Manifestations of
Irritability of neuromuscular system
Tetany—hypertonic muscle contractions , numbnes,
tingling, cramps in extremities, laryngeal spasm,
bronchospasm, carpopedal spasm ( flexion of the
elbows and wrists, dorsiflexion of the feet), seizures
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
Lab studies may reveal calcium levels of 5-6 mg/dL or
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
Use of parathormone IV reserved for extreme
situations due to the probability of allergic reactions
Monitor calcium levels
May need bronchodilators and even ventilator
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
Usually benign tumor
Originates from the chromaffin cells of the adrenal
Any age but usu. Between 40-50 years old
Can be familial
10% are malignant
May be associated with thyroid carcinoma or
parathyroid hyperplasia or tumor
Clinical Manifestations
Headache, diaphoresis, palpitations, hypertension
May have hyperglycemia related to excess epinephrine
Tremors, flushing and anxiety as well
Blurring of vision
Feeling of impending doom
BPs exceeding 250/150 have occurred
Assessment and Diagnostic Findings
 Associated with the 5 H’s—hypertension, headache,
hyperhidrosis, hypermetabolism and hyperglycemia
 Urinary catecholamines and metanephrine are direct and
conclusive tests
 Serum epinephrine and norepinephrine levels will be
 Urinary vanillymandelic acid also diagnostic
 Must avoid coffee, tea, bananas, chocolate, vanilla and
ASA, nicotine, amphetamines, decongestants before 24h
urine testing
 Clonidine suppression test—in normal individual, would
block catecholamine release
 Imaging studies
Elevated HOB
Calcium channel blockers and Beta blockers
Surgical management (manipulation of the tumor can
cause excessive release of catecholamines)
Steroid therapy if adrenalectomy performed
Hypotension and hypoglycemia can occur post-op
Addison’s Disease
Adrenocortical insufficiency
Autoimmune or idiopathic atrophy
Can be caused by inadequate ACTH from pituitary
Therapeutic use of steroids
Muscle weakness
Dark pigmentation
Low sodium levels
High potassium levels
Can result in Addisonian crisis
Addisonian crisis
Circulatory shock
Pallor, apprehension, weak&rapid pulse, rapid
respirations and low blood pressure
Headache, nausea, abdominal pain and diarrhea
Can be brought on by overexertion, exposure to cold,
acute infection, decrease in salt intake
Assessment and Diagnostic Findings
Early morning serum cortisol and plasma ACTH are
performed. Will distinguish between primary and
secondary adrenal insufficiency. In primary, will have
elevated ACTH levels and below normal cortisol
If the adrenal cortex is not stimulated by the pituitary,
a normal response to doses of exogenous ACTH (see
Blood sugar levels and electrolyte values
Restore circulatory status—fluids, steroids
May need antibiotics if infection precipitated crisis
May need lifelong steroid therapy and
mineralocorticoid therapy
May need additional salt intake
Check orthostatics
Daily weights
Aware that stressors can precipitate crises
Medic alert bracelet or similar identification of history
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
Can be caused by bronchogenic carcinoma or other
Manifestations of Cushing’s
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
Assessment and Diagnostic Findings
Overnight dexamethasone suppression test frequently
used for diagnosis
Administered at 11pm and cortisol level checked at
Suppression of cortisol to less than 5mg/dL indicates
normal functioning
Measurement of plasma ACTH (radioimmunoassay) in
conjunction with dexamethasone suppression test
helps distinguish pituitary vs. ectopic sites of ACTH.
MRI, CT and CT also help detect tumors of adrenal or
Medical Management
 If pituitary source, may warrant transphenoidal
 Radiation of pituitary also appropriate
 Adrenalectomy may be needed in case of adrenal
 Temporary replacement therapy with hydrocortisone or
 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.
Primary Aldosteronism or Conn’s
Excessive aldosterone secondary to adrenal tumor
retain sodium and excrete potassium
Results in alkalosis
Hypertension—universal sign of hyperaldosteronism
Inability of kidneys to concentrate the urine
Serum becomes concentrated
Excessive thirst
Hypokalemia interferes with insulin secretion thus will
have glucose intolerance as well
Assessment and Diagnostic Findings
High sodium
Low potassium level
High serum aldosterone level
Low renin level
Aldosterone excretion rate after salt loading is
diagnostic for primary aldosteronism
Renin-aldosterone stimulation test

Surgical removal of tumor
Correct hypokalemia
Usual postoperative care with abdominal surgery
Administer steroids
Monitoring of blood sugar
Control of hypertension with spironolactone
Corticosteroid Therapy
Fludrocortisone (contains both mineralocorticoid and
glucocorticoid) Florinef
COPD exacerbations
Other autoimmune disorders
Dermatologic disorders
Lowest dose
Limited duration
Best time to give dose is in early morning between 7-8
Need to taper off med to allow normal return of renal
Side Effects of Steroids
Hypertension, thrombophlebitis, accelerated
Increased risk of infection
Glaucoma and corneal lesions
Muscle wasting, poor wound healing, osteoporosis,
pathologic fractures
Hyperglycemia, steroid withdrawal syndrome
Moon face, weight gain, acne
Case Study 1
35 year old male presents with BP of 188/112 at a
yearly physical exam. Previous exams noted blood
pressures of 160/94 and 158/92. On questioning,
patient admits to twice a month episodes of
apprehension, severe headache, perspiration, rapid
heartbeat, and facial pallor. These episodes had an
abrupt onset and lasted 10-15 minutes.
Routine hematology and chemistry studies are wnl and
chest xray and ECG are normal.
What is your impression?
What labs would you draw?
Case Study 2
50 year old woman presents with enlargement of left
anterior neck. She has noted increased appetite over
the past month with no weight gain, and more frequent
bowel movements over the same period. Patient feels
jittery at times, experiences palpitations and feels “hot”
a lot recently.
She is 5’8” tall and weighs 150#. Heart rate is 110 and
blood pressure is 110/76.
What might be this patient’s problem?
What lab tests might you draw?
Case study 3
48 year old woman with a past history of mental
illness presents with a new onset of bizarre psychotic
behavior. She had been well over the past two years.
She is 5’5” tall and weighs 138#. Her heart rate is 65,
irreg and BP is 130/75. Exam is normal except that she
is confused to place, time and year. Patient c/o joints
aching and of feeling fatigued.
Lab tests reveal serum calcium level of 13.8mg/dL
(reference range is 8.4-10.1)
Phosphorus is 2.4 (reference range is 2.5-4.5)
What is your diagnosis?
Case Study 4
40 year old deeply tanned woman presents with a 6
month history of increasing fatigue. For the past three
months she has suffered from recurrent URIs, poor
appetite, abdominal cramps, fatigue and diarrhea. She
has lost 25#. She has noted joint pains, muscle
weakness, and has not menstruated for the past 3
Labs reveal blood glucose of 59, Na+ 130, K+ 6.0.
What disorder do you expect?
Case Study #5
 27 year old woman presents with depression, insomnia,
increased facial fullness and recent increase in acne. She
had an episode of depression and acute psychosis following
uncomplicated delivery of normal baby boy 9 months
previously. Her menses have been irregular since their
resumption after the birth (she is not breast feeding). Patient
relates has had several vaginal yeast infections recently.
 Heart rate is 90bpm, BP is 146/100. Her face is puffy and
has acne vulgaris. Thin extremities and with truncal obesity.
 What are your suspicions?
 What labs will you draw?