Assessment and Management of

Patients with Endocrine Disorders

By Linda Self

Glands of the Endocrine System

Hypothalamus
Posterior Pituitary
Anterior Pituitary
Thyroid
Parathyroids
Adrenals
Pancreatic islets
Ovaries and testes

Hypothalamus
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 hormoneovary in female, sperm

in males
Luteinizing hormonecorpus luteum in females,
secretion of testosterone in males
Prolactinprepares female breasts for lactation

Posterior Pituitary
Antidiuretic Hormone
Oxytocincontraction of uterus, milk ejection from

breasts

Adrenal Cortex
Mineralocorticoidaldosterone. Affects sodium

absorption, loss of potassium by kidney

Glucocorticoidscortisol. Affects metabolism,

regulates blood sugar levels, affects growth, antiinflammatory action, decreases effects of stress
Adrenal androgensdehydroepiandrosterone and

androstenedione. Converted to testosterone in the

periphery.

Adrenal Medulla
Epinephrine and norepinephrine

serve as neurotransmitters for sympathetic system

Thyroid
Follicular cellsexcretion of triiodothyronine (T3)

and thyroxine (T4)Increase BMR, increase bone and

calcium turnover, increase response to catecholamines,
need for fetal G&D
Thyroid C cellscalcitonin. Lowers blood calcium
and phosphate levels

Parathyroid
Parathyroid hormoneregulates serum calcium

Pancreatic Islet cells

Insulin
Glucagonstimulates glycogenolysis and

glyconeogenesis
Somatostatindecreases intestinal absorption of

glucose

Kidney
1, 25 dihydroxyvitamin Dstimulates calcium

absorption from the intestine

Reninactivates the RAAS
ErythropoietinIncreases red blood cell production

Ovaries
Estrogen
Progesteroneinportant in menstrual cycle,*maintains

pregnancy,

Testes
Androgens, testosteronesecondary sexual

characteristics, sperm production

Thymus
Releases thymosin and thymopoietin
Affects maturation of T lymphocetes

Pineal
Melatonin
Affects sleep, fertility and aging

Prostaglandins
Work locally
Released by plasma cells
Affect fertility, blood clotting, body temperature

Assessment
Health historyenergy level, hand and foot size

changes, headaches, urinary changes, heat and cold

intolerance, changes in sexual characteristics,
personality changes, others
Physical assessmentappearance 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 testsdetermine how an endocrine gland
responds to stimulating hormone. If the hormone
responds, then the problem lies w/hypothalmus or
pituitary
Suppression teststests 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
disturbances
Basophilic tumors may cause Cushings syndrome
w/features of hyperadrenalism, truncal obesity,
amenorrhea, osteoporosis
Chromophobic tumors90% 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 TumorsAssessment and

Diagnostic Findings
H&P
Vision tests
CT, MRI
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 DIrelates to failure of the renal tubules
to respond to ADH. Can be related to hypokalemia,
hypercalcemia and to medications (lithium
demeocycline)

Manifestations
Excessive thirst
Urinary sp. gr. of 1.001.1.005

Assessment and Diagnostic Findings

Fluid deprivation testwithhold 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
DDAVPintranasal 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 originthiazide 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 originsuch 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 (Lasix),
fluid restriction, I&O, daily wt., lab chemistries

SIADH
Restoration of electrolytes must be gradual
May use 3% NaCl in conjunction with Lasix

Thyroid
T3 and T4
Need iodine for synthesis of hormonesexcess will

result in adaptive decline in utilization called the WolfChaikoff 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
Calcitoninsecreted in response to high levels of
serum calcium, increases deposition in the bone

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 Hashimotos, Graves 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 scanhelps 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

Hypothyroidism
Most common cause is Hashimotos 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

Manifestations
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/Sfatigue, 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
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

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

Hyperthyroidism
Extreme form is Graves disease
Caused by thyroiditis, excessive amount thyroid

hormone, abnormal output by immunoglobulins

Is more common in women

Manifestations of hyperthyroidism
Thyrotoxicosisnervousness, 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

Management
Reduce thyroid hyperactivityusually use radioactive

iodine, antithyroid meds or surgery)

Beta blockers
Can be relapse with antithyroid meds

Pharmacologic Therapy
Irradiation with administration of radioisotope iodine

131initially may cause an acute release of thyroid

hormones. Should monitor for thyroid storm
S/S of thyroid stormhigh fever. Tachycardia,
delirium, chest pain, dyspnea, palpitations, weight loss,
diarrhea, abdominal pain
Management of thyroid stormoxygen, 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
PTUpropylthiouracilblocks 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
Dexamethazonesuppresses release of thyroid
hormones

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

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 hyperparathyroidism is

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

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

Hypoparathyroidism
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
tubules

Clinical Manifestations of
Hypoparathyroidism
Irritability of neuromuscular system
Tetanyhypertonic 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

Trousseaus signcan check with a BP cuff
Chvosteks signtapping over facial nerve causes

spasm of the mouth, nose and eye

Lab studies 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

Adrenals--Pheochromocytoma
Usually benign tumor
Originates from the chromaffin cells of the adrenal

medulla
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

secretion
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 Hshypertension, headache,

hyperhidrosis, hypermetabolism and hyperglycemia

Urinary catecholamines and metanephrine are direct and
conclusive tests
Serum epinephrine and norepinephrine levels will be
elevated
Urinary vanillymandelic acid also diagnostic
Must avoid coffee, tea, bananas, chocolate, vanilla and
ASA, nicotine, amphetamines, decongestants before 24h
urine testing
Clonidine suppression testin normal individual, would
block catecholamine release
Imaging studies

Management
Bedrest
Elevated HOB
ICU
Nipride
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

Addisons Disease
Adrenocortical insufficiency
Autoimmune or idiopathic atrophy
Can be caused by inadequate ACTH from pituitary
Therapeutic use of steroids

Manifestations
Muscle weakness
Anorexia
Dark pigmentation
Hypotension
Hypoglycemia
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
levels.
If the adrenal cortex is not stimulated by the pituitary,
a normal response to doses of exogenous ACTH (see
text)
Blood sugar levels and electrolyte values

Management
Restore circulatory statusfluids, 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

Cushings 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
malignancy

Manifestations of Cushings
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

Assessment and Diagnostic Findings

Overnight dexamethasone suppression test frequently

used for diagnosis

Administered at 11pm and cortisol level checked at
8am
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
pituitary

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.

Primary Aldosteronism or Conns

Syndrome
Excessive aldosterone secondary to adrenal tumor
retain sodium and excrete potassium
Results in alkalosis
Hypertensionuniversal 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

Management
Surgical removal of tumor
Correct hypokalemia
Usual postoperative care with abdominal surgery
Administer steroids
Fluids
Monitoring of blood sugar
Control of hypertension with spironolactone

Corticosteroid Therapy
Hydrocortisone--Cortisol
Cortisone--Cortate
Prednisone--Deltasone
Prednisolone-Prelone
Triamcinolone--Kenalog
Betamethasone--Celestone
Fludrocortisone (contains both mineralocorticoid and

glucocorticoid) Florinef

Indications
RA
Asthma
MS
COPD exacerbations
Lupus
Other autoimmune disorders
Dermatologic disorders

Dosing
Lowest dose
Limited duration
Best time to give dose is in early morning between 7-8

am
Need to taper off med to allow normal return of renal
function

Side Effects of Steroids

Hypertension, thrombophlebitis, accelerated

atherosclerosis
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 58 tall and weighs 150#. Heart rate is 110 and
blood pressure is 110/76.
What might be this patients 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 55 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
months.
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?