Endocrine

 Structures and Functions of the Endocrine System

 Glands: organs in the endocrine system
 The glands secrete hormones and hormones travel through the blood and
exert their action at the site only that they are suppose to exert it at
 Endocrine System Functions
 Communicates through chemical substances (hormones)
 Reproduction
 Growth and development
 Regulation of energy
 Composed of glands and glandular tissues
 Regulated by a feedback system (5 feedback system)
1. Negative feedback system: increase or a decrease in the secretion of a
hormone based on the feedback levels of various factors. For example,
like a thermostat at your house Based on the temperature of the house, it
either increases or decreases. Once it’s at the temperature it’s set for, it
shuts off. Once it drops down again, it starts to work again and exert its
energy.
2. Positive feedback system: increase the target organ action above
normal level. When a woman is in labor, the brain keeps sending oxytocin
to push the uterus above the target level until we get the desired level
(delivery of the baby)
3. Complex: communication via hormones among several glands to turn on
or turn off target organ hormone secretion. The glands communicate back
and forth. The action is going on all at once.
4. Nervous feedback system: initiated by your CNS and it’s implanted by
your sympathetic nervous system. With stress, CNS starts it up, and SNS
kicks in to increase the HR and BP to deal appropriately with the stress.
5. Rhythm feedback system: circadian rhythm. The hormones are secreted
regularly over that 24 hour period.
 Endocrine assessment:
 Past health history: sleeping patterns, coping patterns, eating patterns, are
they energetic? Too tired? Constipation, diarrhea, urine output, activity level?
Able to do their ADLs? How do they cope with everything in general (are they
angry, anxious, do they have any psychosocial problems)
 Medications: OTC, prescriptions, herbals. How much? How often? How long
taking it? Side effects? How does it work for them?
 Past surgical history: anything related to glands, brain surgery, neck surgery,
radiation
 Physical assessment:
 Vital signs: hypo/hyperthermia, hypo/hypertension, bradycardia/
tachycardia
  Height and weight: more concerned about weight. Do they have an
unexplained weight loss or gain. How does that relate to their eating
patterns?
 Head to toe: look at skin (nice, moist), shouldn’t be diaphoretic, dry and
scaly. Nails should be nice and thick (should not thin and brittle). Hair
should be evenly disturbed (no patchy areas of hair anywhere). Eyes
should not be bulging or protruding. Tongue should be normal size, no
speech difficulties, and no recent sleep apnea. Thyroid typically can’t be
felt. If it’s enlarged, do not manipulate it. Note it and let the physician
know (if you manipulate it, extra thyroid hormone can be secreted in
someone who already has hyperthyroidism and can cause a crisis).
Bowel: sounds (hypo/hyperactive), looking for striaes (purple/red
throughout breast, abdomen, buttocks). Any type of edema. Have the
hands or feet grown.
 Psychosocial assessment: are they alert, do they answer questions
appropriate. Do they have trouble paying attention?
 Diagnostic Tests:
 Serum tests
 MRI
 Ultrasounds
 Radioactive iodine uptake
 Thyroid scans
 CT scans
 Gerontologic considerations: decrease hormone production secretion
 Altered hormone metabolism and biologic activity
 Decreased responsiveness of target tissues to hormones
 Alterations in circadian rhythms

Pituitary gland: called the master gland of the body.

 Without the hypothalamus, it wouldn’t work. Pituitary gland and hypothalamus
work together.
 Anterior pituitary: communication is done through a capillary tract
 Posterior: ADH and oxytocin, regulated through a nerve tract

 Anterior pituitary: regulated by hypothalamus

 Secretes TSH (thyroid), ACTH (corticosteroids), FSH (estrogen and the
development of ova in female and sperm in men), LH (ovulation and sex
hormone for males and females), GH (affects all body tissues; growth and
development of the skeletal muscles and long bones), prolactin
 Excess secretion results in increased production of whatever is being
secreted
 Anterior pituitary excess
 ACTH: can cause adrenal insufficiency and shock
  TSH: can cause a thyroid storm
 Growth Hormone Excess
 Overproduction of growth hormone
 Stimulates liver to produce insulin-like growth factor which results in
increased growth of bones and soft tissues
 Usually caused by a benign pituitary tumor
 In children it’s called gigantism
 In adults, it’s called acromegaly
 Acromegaly: overproduction of growth hormone
 Benign pituitary tumor
 CM: thick and oily skin, facial features start to spread, large hands and feet
(b/c bones and tissues grows so thick), large mandible that juts forward and
pushes out, speech difficulty, deepened voice (b/c of hypertrophy of vocal
cords, lot of time the tongue gets larger), joint enlargement (pain can be from
anywhere from mild to crippling), hyperglycemic, sleep apnea (b/c they have
extra soft pharyngeal tissue which causes airway obstruction), visual
disturbances (happens because it takes up a space that doesn’t belong and
presses on the optic nerve – space occupying tumor), atherosclerosis,
cardiomegaly, start seeing symptoms between 20-30. It’s slow progressing,
don’t diagnose it for 7-9 years
 Assessment: history and physical (looking for CM)
 Labs:
 Rely on the IGF (consistent, always get an accurate reading)
 Serum GH (can get different readings)
 Oral glucose challenge test – a challenge test for a pregnant woman.
We give the oral glucose and test their GH at 30, 60, 90, and 120
minutes. At the end of the 120 minutes, when we draw the GH. The GH
decreases, but stops at a certain point and stay elevated (don’t drop
all the way). Typically in normal humans, our GH would fall
dramatically.
 MRI: looking for tumor, how much surrounding area is involved
 CT: localizes your tumor
 Ophthalmologic exam: because it comes close to compressing the optic
nerve
 Nursing Diagnoses:
 Exercise intolerance
 Acute/chronic pain
 Disturbed body image
 Altered sleep pattern
 Insomnia
 Disturbed sensory perception (if optic nerve is compressed)
 Treatment
 Hypophysectomy: go in under the upper lip and under the nose, risk for
meningitis. If it fails to work, we then use radiation.
  Radiation: reduces our levels in 30-70% of patients. It is used in
conjunction with drug therapy
 Drug therapy: octreotide – inhibits the growth hormone
 Surgery:
 Elevate HOB 30 degrees: to decrease pressure so it doesn’t cause CSF
leakage
 Test drainage for CSF, if it is CSF (put patient on bed rest for 72 hours
with HOB up) if it doesn’t resolve, we can take patient back to surgery or
do a lumbar puncture and pull the CSF out
 Frequent neuro checks (if giving pain meds, use them very cautiously)
 Avoid coughing, sneezing, valsalva maneuver because it causes pressure
on the head which can cause a CSF leak
 Watch for signs and symptoms of DI (polyuria, polydipsia-increased
thirst), will reverse itself (not permanent)
 Hypopituitarism: rare disorder
 Number one cause is a tumor, other causes include autoimmune, infections,
trauma, and surgery
 Deficiency in one hormone (selective hypopituitarism), more than one (pan
hypopituitarism)
 Worried about ACTH and TSH (life threatening)
 CM:
 Hypothyroid symptoms: everything slows down, cold intolerance,
constipation, fatigue, lethargy, weight gain, thin brittle nails
 ACTH deficiency: weakness, skin changes, diminished axillary and pubic
hair, hypoglycemia
 LH/FSH: diminished sperm, impotence, decreased facial hair and muscle
mass, diminished menstruation, amenorrhea, decreased sex drive,
decreased breast size
 GH: growth retardation
 Signs and symptoms of tumor (space occupying lesion – visual
disturbances, headache, lose sense of smell, seizures)
 Assessment:
 History and physical exam: looking for SXS related to different hormone
losses
 Labs: vary widely
 MRI/CT: determine where the tumor is, how much is involved
 Treatment:
 Surgery: remove the tumor
 Hormone: life long hormone replacement (based on whatever is missing)

Disorders of the Posterior Pituitary

 SIADH: over secretion of ADH

 Most commonly see it in patients with small cell lung cancer
  Can also see it in tumor, trauma, medications (it’s typically reversible)
 Etiology: we see fluid retention, someone who is gaining weight (won’t see
edema because it’s intravascular not interstitial)
 Decreased serum osmolality
 Dilutional hyponatremia (have normal sodium but have extra fluid, which
dilutes the sodium to make it appear as if we don’t have enough. When
we pull out that water, the sodium goes back to normal)
 Hypochloremia
 Concentrated urine
 Normal renal function
 CM: hyponatremia (125-134) – muscle cramps, thirst, DOE, decreased urine
output, increased weight, dulled sensorium, severe hyponatremia (<120) –
vomiting, cerebral edema, coma, on seizure precautions
 Assessment: watching vital signs, I & O, increased urine specific gravity
(tells us how concentrated the urine is), daily weights, monitor LOC, watch
for SXS of hyponatremia, lay the HOB flat or no more than 10 degrees
(increase venous return to the heart which decreases the release of ADH)
 Treatment: treat underlying cause
 Goal is to restore fluid and electrolyte balance
 At mild hyponatremia – restrict fluid (800-1000 cc a day). We want their
output to be more than input
 Severe hyponatremia – hypertonic saline 3-5%, run it extremely slow,
highly potent. Can give loop diuretics like Lasix if sodium is greater than
125
 We stop the medications that release ADH
 If patient is chronic who have small cell lung cancer, they will always be
on 800-1000 cc per day.
 They need to be aware of ice chips or jello is included in the count.
 Have sodium and potassium in diet.
 Teach SXS of hyponatremia.
 To help dilute their urine, declomycin is given
 Diabetes Insipidus: decrease in ADH
 Dumping urine
 Typically seen after head trauma (more transient, will go away) or cranial
surgery (it’s more likely to stay)
 CM: polyuria – can put out 5-20 L of urine per day, low BP, tachycardia, dry
mucous membranes, poor skin turgor, constipated, fatigue (b/c they are
putting out so much urine), increased serum osmolality, decreased urine
osmolality
 Types
 Central (neurogenic): most common, originates from brain, problem
with the transport of ADH (either the transport of ADH or release of
ADH), more output of urine and more thirst; associated with dehydration
and hypovolemia
  Nephrogenic: kidney, enough ADH but problem with responsiveness to
the kidney; less common; associated with dehydration and hypovolemia
 Primary (psychogenic): least common, excess water intake, associated
with lesions and thirst mechanism in the brain; associated with
hypervolemia and overhydration
 Assessment: history and physical – looking for someone with head trauma
or cranial surgery, looking for dumping urine, looking at labs
 Labs: sodium, potassium, serum and urine osmolality, will have
decreased urine specific gravity (b/c urine is diluted)
 Water deprivation test: tells us whether it is nephrogenic or neurogenic.
We take away water from patient for 8-16 hours. Then there are labs we
do, vitals. When we reach the guidelines, we stop the test. At the time the
patient reaches the point, we give vasopressin (synthetic form of ADH) –
if our patient has neurogenic DI, you will see a rise in urine osmolality. If
we give vasopressin and your patient has nephrogenic DI, nothing will
happen (no response)
 Treatment:
 If it’s neurogenic, we continue to give vasopressin and DDAVP. We want
our urine output to decrease and urine specific gravity to increase
 Fluid replacement (hypotonic) used for both – titrated to replace a urine
output, we replace cc to cc. until urine output is normal
 If your patient has nephrogenic, we given them thiazide diuretics and low
sodium diet. If for some reason, the thiazide diuretic and low sodium diet
doesn’t work, we use a drug called Indocin. Indocin increases renal
responsiveness to ADH (b/c with nephrogenic the kidney response is not
working)
Thyroid Disorders
 We want our patients to be in a euthyroid state (in the middle)

 Hyperthyroidism:
 Sustained increase in synthesis and release of thyroid hormones by the
thyroid gland
 Typically seen in women 20-40 years old, but men get it too
 75% cases are autoimmune – Grave’s disease, don’t know why it happens
(triggered by stressful life events, infection, insufficient iodine supply)
 Associated with toxic nodular goiters (b/c they are related to thyroid)
 Can be multiple or single nodules
 Multiple (over age of 40, equally in men and women), usually benign, not
cancerous
 CM: everything speeds up (CNS, metabolic rate), exophthalmos – impaired
drainage, increased fat and edema in retroorbital tissues, 20-40% of patients
get it
 Cardiovascular: bruit over thyroid (b/c of increased blood supply)
 Systolic hypertension
 Increased CO
  Dysrhythmias
 Cardiac hypertrophy
 AFIB
 GI: increased appetite and thirst, weight loss, diarrhea, splenomegaly,
hepatomegaly
 Integumentary: warm, moist skin, diaphoretic, heat intolerance, clubbing
of fingers (decreased perfusion), thin, brittle nails, hair loss, vitiligo (loss
of pigment in skin)
 Musculoskeletal: fatigue, muscle weakness, muscle wasting, edema,
osteoporosis
 Nervous system: everything speeds up, fine tremors, insomnia, restless,
irritable, mood swings, hyperreflexia, nervousness
 Reproductive system: amenorrhea, impotence, decreased libido,
decreased fertility
 Misc manifesations: heat intolerance, can’t have caffeine or anything spicy
because it will speed up the CNS and potentially go into a thyroid storm,
elevated temperature, exophthalmos, goiter, rapid speech
 Diagnosis: history and physical
 Physical exam and eye exam
 EKG (dysrhythmia, tachycardia, AFIB)
 Radioactive iodine uptake (typically uptake is 2%, for hyperthyroidism, it
is a significant uptake – 35%+)
 Lab tests (T3 and T4 not very useful), TSH will be decreased, free T4 will
be increased
 Complications: if left untreated or has a stressful event, can go into a thyroid
storm
 Thyrotoxicosis (thyroid storm): tachycardia, HF (b/c heart is working
too heart), shock, hyperthermia (105 degrees), restlessness, agitation,
seizures, abdominal pain, N/V, diarrhea, delirium, coma
 Treatment: drugs and support (oxygen, cannula, face mask,
ventilator), fluid replacement, fever reduction (ice pack, cooling
blankets), management of stressors (patient are in a quiet room),
replace fluid and electrolytes)
 Nursing diagnosis:
 Activity intolerance
 Disturbed body image
 Altered nutrition less than body requirements
 Insomnia
 Fatigue
 Medical managements:
 3 primary treatment options:
1. Antithyroid medications
2. Radioactive iodine therapy (RAI)
3. Subtotal thyroidectomy
 We prefer radioactive iodine therapy, but not everyone can have it
 Drug therapy:
 Start with antithyroid drug (PTU, tapazole). They inhibit the synthesis
of the thyroid hormone.
 Improvement is usually seen in 1 to 2 weeks, with best results in
4-8 weeks.
 Typically have to wait for 1-2 months for it to really take effect.
Leave on therapy to 6-15 months.
 At end of 15 months, we take the patient off the medication in
hope that patient’s hyperthyroidism has remised. If that is not the
case, we put them back on medication and do radioactive iodine or
surgery
 Disadvantage: patient noncompliance and increased rate of
recurrence
 PTU: inhibits synthesis of the thyroid hormone and blocks
conversion of T4 to T3, taken TID
 Tapazole: only take once daily
 Iodine: the one you drink.
 Side effect; mucosal swelling, excess salivation, skin changes,
vomiting
 We are trying to decrease the vascularity of thyroid gland. Takes
1-2 weeks to take effect
 Used before surgery to reach euthyroid state. Not used long term.
 Beta-adrenergic blockers: symptom relief. We are trying to decrease
heart rate and get rid of arrhythmias
 Radioactive iodine: treatment of choice. Destroys the thyroid tissue.
We don’t want to destroy all but just enough to stop hyperthyroidism
and let it regenerate. However, 80% of people have the whole thyroid
destroyed. Have to wait 2-3 months for results
 Teach SXS of hypothyroidism and teach them what normal looks
 Nutritional therapy: for a patient who is still hyperthyroid
 High calorie diet (4000-5000 a day) split up in 6 full meals a day
 High protein, high carbohydrates
 Vitamin A
 Thyamine
 Vitamin B6
 Vitamin C
 Avoid caffeine, highly seasoned foods ( to avoid speeding up CNS),
high fiber foods
 Surgery: subtotal thyroidectomy
 Indications:
 Unresponsiveness to drug therapy
 Large goiters causing tracheal compression
 Possible malignancy
  Individual not a good candidate for RAI
 Take 90% of the thyroid out, so that the 10% can regenerate into a
healthy thyroid
 If we take more than 90%, it won’t be able to regenerate and can go
into hypothyroidism
 Advantage: immediate decrease in T3 and T4
 Open or endoscopic
 Before the surgery they will be on antithyroid meds, iodine, and beta-
adrenergic blockers
 Postop complications:
 Hypothyroidism
 Damage or inadvertent removal of parathyroid glands (monitor for
hypocalcemia for first 72 hours – tingling, muscle spams, laryngeal
stridor)
 Hemorrhage (hypotension, tachycardia, might feel like swallowing,
vomit)
 Injury to laryngeal nerve
 Thyrotoxic crisis
 Infection
 Airway obstruction: number one concern, always have oxygen,
suction, and trach kit at bed side
 Postoperative care:
 Assess patient every 2 hours for 24 hours for SXS for hemorrhage,
tracheal compression (irregular breathing, neck swelling, frequent
swallowing, choking)
 Place them in Semi-Fowler’s position – avoid flexion of neck and avoid
tension on suture lines
 Monitor V.S., control pain
 Check for tetany for 72 hours (trousseau’s and chvostek signs), if
patient has laryngeal stridor (treat them with calcium gluconate –
given slow over 5 minutes, put pt. on a monitor)
 Evaluate difficulty in speaking/hoarseness
 Ambulatory and home care:
 Send them to the biweekly for a month and then semiannual
 Decrease caloric intake to prevent weight gain (1200-1500)
 Regular exercise
 Avoid increased environmental temperature (thyroid can’t regenerate
under high temperatures)
 Will be on lifelong thyroid replacement
 Teach SXS of hypothyroidism (everything slowing down, cold,
constipation, lethargy)
 Radioactive iodine therapy: no precautions
 Teach SXS of hypothyroidism
 Hypothyroidism: one of the most common disorders in the U.S.
 Affects 10% of women and 3% of men over the age of 65
 Unless it results after a thyroidectomy, a thyroid ablation, or during
treatment with antithyroid drugs, the onset of symptoms may occur over
months to years
 Natural atrophy of the gland will take months to years for symptoms to show
 Etiology and Pathophysiology:
 Primary: related to the destruction of the thyroid tissue and has to do
with the synthesis of hormones
 Secondary: related to pituitary disease with decreased TSH secretion
 Tertiary: discontinuing thyroid hormone therapy or thyroiditis
 Most common cause in U.S. is atrophy of the gland (hyperthyroid
treatment that destroy the gland or natural atrophy of the gland)
 Most common cause worldwide, it is iodine deficiency
 Atrophy is the end result of Hashimoto’s thyroiditis and Grave’s disease:
are autoimmune disease that destroy the thyroid
 Result of treatment for hyperthyroidism
 Amiodarone and lithium decrease the TSH production
 Cretinism: baby hypothyroidism, decrease function in thyroid
 A test called PKU is taken and sent off to the state and the state
evaluates it and sends it back to the doctor
 CM: depend on severity (how much damage is done to the gland), the age of
onset, and duration
 Body system slows down
 Cardiovascular: decreased CO, decreased cardiac contractility,
bradycardia, anemia (decreased erythropoietin level), cobalamin, iron,
folate deficiencies (causes easy bruises), increased serum cholesterol and
triglycerides can cause atherosclerosis; Has an effect on respiratory
system
 Respiratory: DOE, decreased exercise tolerance
 Neurologic: become fatigued and lethargic, personality and mood
changes, impaired memory, slowed speech, decreased initiative and
somnolence, sleep a lot
 Reproductive: menorrhagia – irregular vaginal bleeding or inovulatory
(infertile)
 GI: decreased motility causing constipation, achlorhydria (decreased
gastric secretion)
 Integumentary: hair loss, dry coarse skin, brittle nails, hoarseness,
muscle weakness and swelling, weight gain, cold intolerance
 If it’s untreated, we can develop myxedema coma: life-threatening issue,
causes puffiness, periorbital edema, masklike effect
 It causes mental sluggishnesss and drowsiness and can go into a coma
 Can be precipitated by infection, drugs, cold or trauma
  We don’t want our patient to have barbituates, opioids, tranquilizers
because they stay in the system longer and can put patient in a coma
 Low temperature, hypotension, hypoventilation (a lot of them will end
up on ventilator)
 Nursing care: putting patient on ventilator, O2 support, cardiac
monitoring, IV thyroid hormone replacement, if hyponatremic,
hypertonic saline may be administered, monitor core temperature
(warm them up), vitals (rise back to normal – shouldn’t be
bradycardia), weight, I & O
 We want to see our cardiovascular, mental alertness, and energy
level to normal so that we can get the patient off the ventilator
 Diagnosis: history and physical examination (looking for the all the CM in
which the body system slows down, those patients who had treatment for
hyperthyroidism)
 Labs: elevated TSH, decreased T3 and T4
 High cholesterol and triglycerides, anemia
 Nursing Diagnosis: knowledge deficit
 Risk for impaired skin integrity
 Noncompliance
 Impaired memory
 Fatigue
 Constipation
 Disturbed body image
 Altered nutrition more than body requirements
 Activity intolerance
 Drug therapy:
 Levothyroxine (synthroid): have to take it regularly
 Watching for palpitations
 With normal patients, we draw labs every 4 weeks and adjust the
level accordingly
 With an elderly or cardiac compromised, we start with a low dose and
adjust it accordingly because too much synthroid requires an
increased oxygen demand which those patients are incapable of
 Will be drawing labs for the heart and do an EKG
 Nursing Management – Health promotion:
 High risk populations are screened (patients who have had
hyperthyroidism treatment, who have SXS of the system slowing down) –
do not require acute nursing care; typically treated on an outpatient basis
 Explain why they are getting thyroid hormone because their body is not
able to produce it and it’s lifelong replacement
 Teach measures to prevent skin breakdown (use soap sparingly and use
lotion because they dry flaky skin)
 Emphasize need for a warm environment – because they are always going
to be cold (they need extra layers of clothes)
  Caution to avoid sedatives or use lowest dose possible
 Discuss measures to minimize constipation (avoid enemas because of
vagal stimulation) – high fluids, exercise, increased fiber
 Watch for orthopnea, dyspnea, rapid pulse, palpitations, nervousness,
insomnia (hyperthyroidism symptoms as result of too much medication)

Parathyroid Disorders

 Hyperparathyroidism: increased secretion of PTH and thus your calcium

increases, decreased phosphate level
 CM: weakness, loss of appetitie, constipation, fractures, nephrolithiasis
(kidney stones)
 Can lead to renal failure and cardiac changes if left untreated
 Primary: due to increased secretion of PTH leading to disorders of the
calcium, phosphate, and bone metabolism. Typically a benign tumor
 Secondary: compensatory response to conditions that induce or cause
hypocalcemia. Usually chronic kidney disease
 Tertiary: hyperplasia of the parathyroid gland. Typically a patient who has
chronic kidney disease, been on long-term dialysis, had a kidney transplant
 Labs: increased PTH and calcium, decreased phosphate
 Bone density measurements: DEXA and QUS scan to detect bone loss,
osteoporosis
 MRI, CT, Ultrasound – looking for tumor
 Collaborative Care:
 Primary thing is to relieve symptoms and prevent complications caused
by excess PTH
 Surgery:
 Parathyroidectomy: whole parathyroid removed; no PTH, calcium
levels can’t be normalized; will be on calcium supplements
 Partial parathyroidectomy: still have part level, can still control
calcium levels because we still have some PTH being secreted
 Auto transplantation of normal parathyroid tissue in forearm:
save some parathyroid gland before parathyroidectomy and implant
on forearm (first choice), will secrete PTH and normalize calcium
levels
 Nonsurgical therapy: annual exam with labs, watching out calcium
levels, x-rays, high fluids (to flush kidneys out) and moderate calcium
intake
 Drugs: Biphosphonates: inhibits osteoclastic bone reabsorption and
rapidly normalize our calcium levels
 Nursing Management:
 Major complications after surgery: hemorrhage (can be choking or
vomiting blood) and fluid and electrolyte disturbances
 Watching for tachycardia, hypotension
  Monitor for tetany (chvostek’s and trousseau’s signs – muscle stiffness,
numbness, tingling, laryngeal stridor) – treat it with calcium gluconate
 Encourage mobility
 Monitoring intake and input
 If surgery is not performed, we are adding our exercise program
 Hypoparathyroidism: decreased PTH and calcium, increased phosphate
 Most common cause is accidentally removing the parathyroid glands with
neck surgery or thyroidectomy
 CM: tetany, dysphagia (feel like their throat is constricted), laryngospasms
 Labs: decreased serum calcium, decreased PTH, increased phosphate
 Nursing Management:
 Primary management: calcium gluconate, slowly IV push, and put them
on a cardiac monitor
 Make sure you have a patent IV line and if you give calcium in a bad
site, it can cause necrosis and sloughing of the tissues
 Rebreathing (decreases signs and symptoms of tetany so that we can
treat them)
 Teach diet – calcium supplements (do not give PTH replacement b/c it’s
expensive), avoid foods that are high in oxalic acid (spinach, rhubarb) and
phytic acid (bran, whole grains) because these decrease calcium
absorption, vitamin D. This will be a life-long supplement

Adrenal Gland Disorders

 Adrenal cortex steroid hormones:

 Glucocorticoids: regulate metabolism and increase our blood glucose; they
are critical to our physiologic stress response
 Mineralocorticoids: regulate sodium and potassium balance
 Androgen: growth and development and sexual activity in adult women

 Cushing’s Syndrome: moon face, real puffy, round, red, edematous

 Etiology and pathophysiology: caused by excess of corticosteroids, can be a
tumor (ACTH secreting tumor, lung or pancreas tumor)
 CM: big belly, muscle wasting, skin is thin, moon face, easily bruised, put on
paper tape because skin is fragile, moon face, cervical area (buffalo hump),
trunk (centripetal obesity), transient weight gain (because we hold on to
sodium and thus hold on water), hyperglycemia (increased gluconeogenesis
by the liver), protein wasting (osteoporosis, muscle wasting which leads to
weakness, fractures, ataxic, gait changes), loss of collagen, delayed wound
healing, easily bruised, insomnia, irrationality, psychosis
 When a person is on steroids, they are at risk for infection
 Mineralocorticoid excess may cause hypertension secondary to fluid
retention
  Adrenal androgen excess may cause pronounced acne, female features in
men and male features in women
 Adrenal carcinomas will cause menstrual disorders and hirsutism in
female; gynecomastia and impotence in men
 Purple red striae on abdomen, breast, or buttocks
 Nursing assessment:
 Subjective data:
 Past health history: pituitary tumor, adrenal, pancreatic, or
pulmonary neoplasms, GI bleeding, frequent infections, use of
corticosteroids
 Functional health patterns: malaise, weight gain, anorexia, polyuria,
prolonged wound healing, easy bruising, weakness, fatigue, insomnia,
headache, back, joint, bone and rib pain, poor concentration and
memory, negative feelings regarding appearance, amenorrhea,
impotence, decreased libido
 Objective data: look at them and see all the manifestations
 Diagnosis:
 Assessment: clinical presentation is the first indication; history and
physical
 Labs: 24 hour urine collection for free cortisol – it will be elevated if they
have Cushing’s disease. For this test, the patient has to be stress free for
24 hours
 ACTH levels elevated
 CT/MRI – to look for tumor
 Nursing Diagnosis: risk for falls
 Disturbed for body image
 Risk for infection
 Risk for impaired skin integrity
 Disturbed sleep pattern
 Self-esteem
 Knowledge deficit
 Altered nutrition more than body requirements
 Impaired sexual function
 Medical management:
 Primary goal is to normalize hormone secretion
 If it’s a tumor, we do surgery and take out the tumor
 If it’s caused by corticosteroids, we take them off corticosteroids (we
need to taper – slowly take them off), decrease the dose, move them to
every other day therapy
 Before they go to surgery, we take care of BP, electrolyte imbalances, we
try to correct protein deficiency, teach them what they are going to do
before and after surgery (incentive spirometer, getting up and moving,
SCDs, turning, coughing and deep breathing)
 Teach about medication side effects
  Watch V/S (cannot be hypertensive), weights (because of high
corticosteroids – holding on to sodium and water)
 Watch hypertension – high risk for hemorrhage
 Elevated glucose because in surgery they will receive a high dose of
corticosteroids until they are able to make their own. High dose
corticosteroids will cause risk for infection
 Meticulous skin care
 Will be on a high protein diet
 Correct fluid and electrolyte imbalance
 Medical alert bracelet
 Addison’s Disease: focused on primary adrenocortical insufficiency: all three
adrenal corticosteroids are decreased (glucocorticoids, mineralocorticoids, and
androgens)
 Etiology and Pathophysiology: autoimmune response
 Can also be caused by TB, infarction, fungal infections, AIDS (treatments
used for AIDS), metastatic cancer, iatrogenic Addison’s disease may be
due to adrenal hemorrhage (caused by anticoagulant therapy)
 Occurs in adults <60 years old
 Affects both genders equally
 CM: symptoms are so vague, usually does not become evident until 9-% of
adrenal cortex is destroyed; progressive weakness, fatigue, weight loss,
anorexia, skin hyperpigmentation
 Does not become evident until 90% of adrenal cortex is destroyed
 Disease advanced before diagnosis
 Skin hyperpigmentations – one thing that distinguishes it if patient does
develop it
 Darkening of areas, over joints, over palms of hands, areas exposed to
sun
 Other misc CM: orthostatic hypotension, hyponatremia, hyperkalemia,
N/V, diarrhea, irritability, depression
 Addisonian crisis: if left untreated, can be typically triggered by stress
(running a mile, infection, getting a tooth pulled, death, birth of child, etc),
sudden withdrawal of corticosteroid therapy, adrenal surgery, and following
sudden pituitary gland destruction
 CM: hypotension, tachycardia, dehydration, hyponatremia, hyperkalemia,
hypoglycemia, fever weakness, confusion
 Diagnosis:
 Subnormal levels of cortisol
 Test electrolytes
 EKG: can have hyperkalemia (increased T waves)
 CT/MRI: localize a tumor
 Collaborative care: give hydrocortisone therapy in an emergency situation
 If there is an emergency in hospital, it will be IV
 If it’s at home, it’s given IM
  Take glucocorticoids twice a day and increase in times of stress (they
have to double or triple it in events of stress)
 Safer to overdose than take a lower dose
 In crisis: we are doing shock management, supporting the airway,
watching V/S, high dose hydrocortisone replacement, high fluid volumes
if hypotensive, watching fluids and electrolytes
 Acute intervention: frequent assessment necessary (every 30 mins –
4 hours for first 24 hours), take daily weights (b/c they will retain
sodium and water), protect against infection, take every dose
diligently, assist with daily hygiene, protect from all extremes
(anything that will cause stress – light, noise, temperature)
 Discharged before maintenance dose reached
 Have take full dose and be compliant
 Instruct follow-up appointments
 Ambulatory and home care management:
 Glucocorticoids are given in 2 doses (2/3 in morning, 1/3 in afternoon)
 Mineralocorticoids are given once a day
 Long term care includes need for extra medication, stress management
 Stress management: yoga, therapist, etc.
 Stressful managements which require doubling doses include fever, cold,
flu, running a mile, tooth extraction, physical exertion, death, divorce
 Teach SXS of corticosteroid deficiency and excess and when to contact
HCP
 Always wear a medical alert bracelet (so people know they need IM
hydrocortisone)
 Provide handouts on drugs that increase need for glucocorticoids
 Instruct on how to take BP and report findings
 Carry emergency kit with needle, syringe, IM hydrocortisone, and
instructions (teach patient and others how to give IM injection)
 Corticosteroid therapy: don’t use them long term unless we actually have to
 Use short term for anti-inflammatory effect
 Effects: anti-inflammatory action, immunosuppression, maintenance of
normal BP (because they help retain sodium and water), carbohydrate and
protein metabolism
 Take them in morning with food to reduce stomach irritation
 Must not be stopped abruptly
 Can cause corticoid-induced osteoporosis
 Hyperaldosteronism:
 Excessive aldosterone secretion resulting in sodium retention and potassium
and hydrogen ion excretion
 Hallmark disease is hypertension with hypokalemic alkalosis
 Primary: adrenocortical tumor, 1% of our cases
 Secondary: occurs in response to nonadrenal cause of elevated aldosterone
levels
  CM: hypertension, hypernatremia, headache, hypokalemia, muscle weakness,
fatigue, cardiac dysrhythmias, glucose intolerance, metabolic alkalosis that
may lead to tetany
 Typically see patients who are hypertensive and hypokalemic but they
are not on diuretics
 Diagnosis:
 Labs: elevated aldosterone levels
 If we do not find a tumor with MRI/CT, we do 18-
hydroxycorticosterone test (have to be on overnight bedrest, levels
will be evelated)
 MRI/CT: localize the tumor
 Surgery:
 Adrenalectomy: open or laproscopic
 Pre-op: low-sodium diet, antihypertensive agents, potassium-sparing
diuretics (don’t give them potassium supplements)
 Nursing Care: assess fluid and electrolyte status and cardiovascular status
before and after surgery
 Monitor BP frequently before and after surgery (after surgery 80% are
cured, 20% still have hypertension)
 Teach side effects of the meds
 Teach SXS of hyperkalemia and hypokalemia
 How to manage BP at home and when to call physician
 Watch for bleeding, low BP, tachycardia

 Pheochromocytoma: rare, 0.1%

 Tumor of adrenal medulla, when it happens, excessive catecholemines are
released and causes severe episodic hypertension
 If left untreated, it can cause hypertensive encephalopathy, diabetes,
cardiomyopathy, and death
 CM: severe, episodic hypertension, Triad: severe pounding headache,
tachycardia with palpitations, profuse sweating. Diagnose is often missed
because it’s 0.1%
 Diagnosis: urinary fractionated metanephrines and catecholamines in 24-
hour collection which will be elevated
 Plasma catecholamines are elevated during the attack (rest of the time
they are not going to be elevated)
 CT/MRI: tumor localization
 Medical Management:
 Surgery: removal of tumor; watch vitals, hypotension, fluid and
electrolytes, tachycardia, signs of bleeding, put them on calcium channel
blockers to control BP, beta blockers for dysrhythmias and tachycardia
 10-30% will still have hypertension, 70-90% of patients will be cured
 Demser (metyrosine) – used if we can’t do surgery, diminishes the
catecholamine production
 If patient is cured after surgery, the medications won’t be used anymore
 Monitor BP
 Make patient comfortable
 Give emotional support and follow up care
 Monitor BP at home (not a guarantee they are cured)
 Monitor glucose
 Difference between DI & SIADH

DI SIADH
 Decreased ADH  Increased ADH
 Increased urine output  Retaining fluid – no edema (vascular)
 Increased thirst (dehydration – poor  Low Na (dilutional hyponatremia)
skin turgor, dry mucous membranes,  125-134 Na (restrict fluid 800-1000
shock, low BP, increased HR cc/day), loop diuretics
 Three types:  <120 Na – 500 fluid restriction, give
1. Neurogenic: 3-5% hypertonic saline, give it slowly
dehydrated/hypovolemia because we can put them into
2. Nephrogenic: hypernatremia
dehydrated/hypovolemia  Head trauma/drugs: transient
3. Psychogenic:  Small cell: chronic, give declomycin
overhydration/hypervolemia to dilute urine
 To differentiate b/w neuro and
nephro, we do water deprivation test
 Neurogenic: vasopression, DDAVP
 Nephrogenic: low Na diet, thiazide
diuretics, Indocin if diet and diuretics
doesn’t work
 We want to see decreased urine
output, and increased specific gravity
 Review after lecture

 Two disorders related to adrenal gland?

 Cushing & Addison
 Signs and symptoms of Cushing’s
 Moon face, purple striae, buffalo hump, centripetal obesity, big belly
 Diagnosis for Cushing syndrome?
 Risk for infection, body image disturbance, nutrition more than body
requirement, knowledge deficit, impaired sexual function, fatigue, anxiety
 Hyperpigmentation is seen in what?
 Addison’s Disease
 Why do we mostly see an Addisonian crisis?
 Stress
 What are we going to with medications in Addisonian crisis?
 Increase, better to overdose than under-dose
 What is in the emergency kit for Addison patients?
 Needle, syringe, IM hydrocortisone, instructions
 Signs and symptoms of hyperthyroidism?
 Everything speeds up, exophthalmos, weight loss, tachycardia, heat
intolerance, insomnia, hunger
 What kind of diet are we having with hyperthyroidism?
 High calorie (4000-5000) in 6 full meals a day, protein, vitamin A, C, B6,
thiamine, carbohydrates
 No fiber, no spicy food
 Signs and symptoms of hypothyroidism?
 Cold intolerance, weigh gain, lethargy, hypotension, bradycardia
 What do we use to treat hypothyroidism?
 Synthroid – lifelong treatment
 What drug should be avoided with a patient with hypothyroidism?
 Sedatives, tranquilizers, valium, barbiturates
 T/F: Corticosteroid therapy is long-term
 False
 Endocrine disorder that’s severe episodic hypertension?
 Pheochromocytoma
 Patient states he has gone up a shoe size in the past year. What do you suspect?
 Acromegaly
 What do we do a hypophysectomy for?
 Acromegaly
 What are nursing interventions after hypophysectomy?
 Elevate the head of the bed
 No coughing, no sneezing, no valsava maneuver to avoid pressure so it
doesn’t cause CSF leakage
 Frequent neuro checks
 What condition are we observing for that’s transient and related to the fact that
we have cranial involvement after hypophysectomy?
 Diabetes Insipidus (DI) (it will resolve itself)
 Signs and symptoms of acromegaly?
 Jutting jaw, hyperglycemia, increase in hands and feet, thick oily skin,
deepened voice, big tongue, sleep apnea
 Nursing Diagnosis for acromegaly?
 Disturbed body image, insomnia, activity intolerance, ineffective breathing
pattern, acute pain, ineffective health management, disturbed sensory
perception (b/c optic nerve is compressed – space occupying tumor)
 T/F: SIADH is reversible with head trauma or drugs?
 True