Disorders of Anterior Pituitary Gland

Acromegaly

Definition
Acromegaly is a rare disorder of excessive bone and soft tissue
growth due to elevated levels of growth hormone. In young children,
prior the completed fusion and growth of bones, excessive growth
hormone can cause a similar condition called gigantism.
Causes
In most cases, acromegaly is caused by over-secretion of growth
hormone (GH) produced by a benign tumor of the pituitary gland. The
pituitary gland is a small gland located at the base of the brain that
produces many hormones. In a small number of cases, malignant
tumors of other organs (pancreas, adrenal, lung) may be the source of
excess GH.
Risk Factors
Some rare cases of acromegaly are hereditary.
The average age of diagnosis is 40-45 years old.

Symptoms
Symptoms usually develop very slowly over time.
Acromegaly can cause serious complications and premature death if
not treated.
In children, excess GH production causes elongation of the bones and
associated soft tissue swelling. If not treated, children with this
disorder can grow to a height of 7-8 feet.
Symptoms and complications in adults may include the following:
Abnormally large growth and deformity of the:
Hands (rings no longer fit)
Feet (need a bigger size shoe)
Face (protrusion of brow and lower jaw)
Jaw (teeth do not line up correctly when the mouth is
closed)
Lips
Tongue
Carpal tunnel syndrome
Skin changes, such as:
Thickened, oily, and sometimes darkened skin
Severe acne
Excessive sweating and offensive body order due to
enlargement of the sweat glands
Deepening voice due to enlarged sinuses, vocal cords, and soft
tissues of the throat
Fatigue and weakness in legs and arms
Sleep apnea
Arthritis and other joint problems especially in the jaw
Hypothyroidism
Enlargement of the liver, kidneys, spleen, heart, and/or other
internal organs, which can lead to:
Diabetes
High blood pressure
Cardiovascular disease
In women:
Irregular menstrual cycles
Galactorrhea (abnormal production of breast milk) in 50% of
cases
In men:
In about 50% of cases, impotence
Diagnosis
Blood tests will be done to measure the level of insulin-like growth
factor (IGF-I), growth hormone releasing hormone (GHRH) , and other
pituitary hormones.
A glucose tolerance test may also be given to see if the GH level drops
it will not drop in cases of acromegaly.
If these tests confirm acromegaly, the following may be done to locate

the tumor that is causing the disorder:

Head CT Scana type of x-ray that uses a computer to make pictures
of the inside of the brain and surrounding structures
MRI Scan
Nursing Diagnosis
Disturbed Body Image related to anxiety over thickened skin and
enlargement of face, hands, and feet.
Ineffective Coping related to change in appearance.
Disturbed Sensory Perception
Disturbed Sleeping Pattern related to soft tissue swelling
Fluid Volume Deficit
Anxiety related to change in appearance
Knowledge Deficit
Treatment Goals
Reduce production of GH to normal levels
Stop and reverse the symptoms caused by over-secretion of GH
Correct other endocrine abnormalities (thyroid, adrenal, sex organs)
Reduce the tumor size
Treatment may include:
Surgery
Surgical removal of the pituitary tumor, or other tumor, that is believed
to be causing acromegaly may be done. In most cases, this is the
preferred treatment.
Radiosurgery
Radiosurgery is the use of highly focused external beams of radiation
to shrink the tumor. It is used most often in patients who do not
respond to conventional surgery or medications.
Radiation Therapy
Radiation therapy is used in combination with either medical and/or
surgical treatment.
Medication
Drugs may be given to reduce the level of GH secretion from the
pituitary gland. These include:
Cabergoline (Dostinex)given orally
Pergolide (Permax)given orally
Bromocriptine (Parlodel)may be given before surgery to shrink tumor
Octreotide (Sandostatin)given by injections
Pegvisomantgiven by injections for patients not responding tother
forms of treatment
Medications must often be combined with other therapies to treat
larger tumors affecting surrounding structures.
Prevention
There are guidelines for preventing acromegaly.
Early diagnosis and treatment, however, will help prevent serious
complications, some of which are irreversible.

Definition
A Hypothyroidism is a condition in which the thyroid gland does not
make enough thyroid hormone. The most common cause of
hypothyroidism is inflammation of the thyroid gland, which damages
the glands cells. Autoimmune or Hashimotos thyroiditis, in which the
immune system attacks the thyroid gland, is the most common
example of this. Some women develop hypothyroidism after pregnancy
(often referred to as postpartum thyroiditis).

Hypothyroidism is a hypothyroid state resulting from a hyposecretion

of the thyroid hormones T4 and T3.
Hypothyroidism is characterized by decreased rate of body
metabolism.
Causes
Hypothyroidism can be a primary disorder that results from disease in
the thyroid gland itself or a secondary or tertiary disorder. In most
cases, hypothyroidism occurs as a primary disorder and results from
the loss of thyroid tissue, which leads to inadequate production of
thyroid hormones (primary hypothyroidism). It is most frequently
autoimmune in origin but can also be related to iodine deficiency.
Secondary hypothyroidism, which occurs in only 5% of cases, is caused
by a failure of the pituitary gland to stimulate the thyroid gland or a
failure of the target tissues to respond to the thyroid hormones.
Tertiary hypothyroidism is caused by failure of the hypothalamus to
produce thyroid-releasing factor.
The most common cause of goitrous hypothyroidism in North America
is Hashimotos disease, which causes defective iodine binding and
defective thyroid hormone production. Hashimotos disease is common
in the same family and is considered an autoimmune disorder leading
to chronic inflammation of the thyroid gland and hypothyroidism but
can also lead to hyperthyroidism.
Risk Factors
Age over 50 years
Being female

Excess of Tropic Hormones

In addition to GH, the pituitary also secretes prolactin,
adrenocorticotropic hormone (ACTH), thyroid-stimulating
hormone (TSH), and ADH.
Prolactinomas are among the most common type of pituitary
adenomas.
o Women with prolactinomas frequently experience
galactorrhea, anovulation, infertility, oligomenorrhea or
amenorrhea, decreased libido, and hirsutism.
In men, impotence and decreased sperm density and libido may
result.
Compression of the optic chiasm can cause visual problems and
signs of increased intracranial pressure, including headache,
nausea, and vomiting.
Because prolactinomas do not typically progress in size, drug
therapy is usually the first-line treatment.
The dopamine agonists cabergoline and bromocriptine have
successfully been used to treat prolactinomas.
Surgery may be done depending on the extent and size of the
tumor.
Radiation therapy may be used to reduce the risk of tumor
recurrence for patients with large tumors.
Hypo function of Pituitary Gland
Hypopituitarism is a rare disorder that involves a decrease in one or
more of the pituitary hormones.
The anterior pituitary gland secretes ACTH, TSH, FSH, LH, GH,
and prolactin.
The posterior pituitary gland secretes ADH and oxytocin.
A deficiency of only one pituitary hormone is referred to as
selective hypopituitarism.
Total failure of the pituitary gland results in deficiency of all
pituitary hormonesa condition referred to as
panhypopituitarism.
The most common hormone deficiencies associated with
hypopituitarism involve GH and gonadotropins (i.e., LH, FSH).
Etiology
Theusualcauseofpituitaryhypofunctionisapituitarytumor.
Autoimmunedisorders,infections,pituitaryinfarction(Sheehansyndrome),

ordestructionofthepituitarygland(fromtrauma,radiation,orsurgical
procedures).
AfricanAmericanshaveahigherincidenceofpituitaryadenomasthan
otherethnicgroups.

Anteriorpituitaryhormonedeficienciescanleadtoendorganfailure.
DeficienciesofTSHandACTHarelifethreatening.
ACTHdeficiencycanleadtoacuteadrenalinsufficiencyandshock.
Hypovolemic shock is due to sodium and water depletion.

Clinical Manifestations and Diagnoses

Earlymanifestationsassociatedwithaspaceoccupyinglesioninclude

headaches,visualchanges(decreasedvisualacuityordecreasedperipheral
vision),lossofsmell,nauseaandvomiting,andseizures.
Inadditiontoahistoryandphysicalexamination,diagnosticstudiessuchas
MRIandCTareusedtoidentifyapituitarytumor.
Laboratorytestsfordiagnosinghypopituitarismvarywidely,butgenerally
involvethedirectmeasurementofpituitaryhormones(e.g.,TSH)oran
indirectdeterminationofthetargetorganhormones(e.g.,triiodothyronine
[T3],thyroxine[T4]).

Collaborative Management
The treatment for hypopituitarism often consists of surgery or
radiation therapy followed by lifelong hormone therapy.
Hormone replacement of lacking hormone.
Somatropin (Omnitrope, Genotropin, Humatrope), which is
recombinant human GH, is used for long-term hormone therapy
in adults with GH deficiency.

o These patients respond well to GH replacement and

experience increased energy, increased lean body mass, a
feeling of well-being, and improved body image.
o Mild to moderate side effects of GH include fluid retention
with swelling in the feet and hands, myalgia, joint pain, and
headache.
o GH is given daily as a subcutaneous injection (preferably in
the evening). The dosing is variable because it is adjusted
based on symptoms, IGF-1 levels, and the development of
adverse effects.
Although gonadal deficiency is not life threatening, hormone
therapy is offered to improve sexual function and general wellbeing.
o This therapy is contraindicated in individuals with certain
medical conditions, such as breast cancer, phlebitis, and
pulmonary embolism in women and prostate cancer in
men.
Estrogen and progesterone replacement therapy may be
indicated for hypogonadal women to treat hot flashes, vaginal
dryness, and decreased libido.
Testosterone is used to treat men with gonadotropin deficiency.
The benefits achieved with testosteronetherapyincludeareturnof

malesecondarysexcharacteristics;improvementinlibido;andincreased
musclemass,bonemass,andbonedensity.
Disorders of Posterior Pituitary Gland
Hormones secreted in POSTERIOR ADH and oxytocin
2 primary problems with ADH is either over or under production of it.
Over production SIADH
Under production DI
Syndrome of Inappropriate Antidiuretic Hormone
Etiology and Patho
o Abnormally high production or sustained secretion of ADH
o In SIADH ADH is released despite normal or low plasma
osmolarity
o Disorder is characterized as fluid retention, serum
hypoosmolality, dilutional hyponatremia, hypochloremia,
concentrated urine in presence or normal or INCREASED
intravascular volume and normal renal function
o More commonly in older adults
o The MOST common cause is malignancy, esp small cell lung
cancer
o It is chronic when associated with tumors or metabolic
diseases

o TABLE 50-2 PG 1193

Clinical Manifestations and Diagnostic Studies
o ADH increases permeability of renal distal tubule and
collecting duct, which leads to the reabsorption of water into
circulation
o Consequently extracellular fluid volume expands, plasma
osmolality declines, glomerular filtration rate increases and
sodium levels decline (dilutional hyponatremia)
Hyponatremia may cause muscle cramping, pain and
weakness
INITIALLY pt will display THIRST, dyspnea on exertion,
and fatigue
o Pt with SIADH experiences low urine output and increased
body weight
As the serum sodium levels falls (usually below 120
mEq/L), manifestations become more severe and
including vomiting, abdominal cramps, muscle
twitching, and seizures
As plasma osmolality and serum sodium DECREASE
MORE cerebral edema lethargy, confusion, H/A,
seizures and coma
o The Diagnosis of SIADH is made by simultaneous
measurements of urine and serum osmolality
Dilutional hyponatremia is indicated by serum sodium
less than 134 mEq/L, serum osmolality less than 280
mOsm/kg and a urine specific gravity greater than
1.025.
Serum osmolality much LOWER than urine osmolality
inappropriate excretion of concentrated urine in the
presence of dilute serum
Nursing and Collaborative Management
o Individuals at risk and those who have confirmed SIADH be
alert for low urine output with high specific gravity, a sudden
weight gain without edema or a decreased serum sodium
level
o Monitor I&Os, VS, and heart/lung sounds
o Observe for signs of hyponatremia seizures, N/V, muscle
cramping, and decreased neuro function
o Once SIADH is diagnosed, Tx is directed at underlying cause
o Medications that stimulate release of ADH should be AVOIDED
or discontinued
o If symptoms are mild and serum sodium is more than 125
mEq/L, only tx may be fluid restriction of 800-1000 ml/day

This restriction should result in gradual reductions in

weight, a progressive rise in serum sodium
concentration and osmolality, and s/s improvement
In acute care setting restrict pts total fluid intake to NO
MORE THAN 1000 mL/day (including fluids taken with
medications) and obtain daily weights
Position head of the bed flat or elevated no more than
10 degrees to enhance venous return to the heart and
INCREASE left atrial filling pressure, thereby reducing
the release of ADH
Frequently turning, positioning, and ROM exercises (if pt
is bedridden) are important to maintain skin integrity
and joint mobility
Protect the pt from injury (assist with ambulation, bed
alarm) because of the potential for alterations in mental
status
Implement seizure precautions
Provide frequent oral care and distractions to decrease
discomfort related to thirst from fluid restrictions
In case of severe hyponatremia (less than 120) esp with neuro
s/s like seizures IV hypertonic saline solution (3-5%) may
slowly be admin
Loop diuretic like furosemide (Lasix) may be used to
promote diuresis but ONLY IF SERUM SODIUM is at
LEAST 125 because you may loss more sodium
b/c lasix increases loss of potassium, calcium, and
magnesium losses, supplements may be needed
Vasopressin receptor antagonist Tolvaptan (Samsca) and
Conivaptan (Vaprisol) are used to treat euvolemiahyponatremia in hospitalized pts
Monitor closely to prevent rapid correction of serum
sodium
Assist the patient with Chronic SIADH in self-management of
tx regimen
In chronic SIADH fluid restriction of 800-1000 mL/day
is recommended
The degree of restriction may be difficult so
Decmeclocycline (Declomycin) may be
administered
o This drug blocks the effect of ADH on renal
tubules, resulting in a more dilute urine
Use of ice chips or sugarless chewing gum helps
decrease thirst
Have pts weight done daily to monitor changes in fluid
balance

o Teach pts to supplement diet with sodium and potassium esp

if they have loop diuretic
o Solutions of these electrolytes must be well diluted to prevent
GI irritation and damage
o They are best taken at meal time to allow mixing with and
dilution by food
o Teach pt s/s of fluid and electrolyte imbalances, esp those
involving sodium and potassium

Diabetes Insipidus
Etiology and Patho
o DI is caused by deficiency in production or secretion of ADH or
a decreased renal response to ADH
o The decrease in ADH results in fluid and electrolyte
imbalances caused by increased plasma osmolality
o Depending on the cause, DI may be transient or a chronic,
lifelong condition
Clinical Manifestations
o DI is characterized by polydipsia and polyuria
o The primary characteristic is the excretion of large quantities
of urine (2-20 L/day) with a very low specific gravity (less than

o
o
o
o

1.005) and urine osmolality is ELEVATED (usually greater than

295 mOsm/kg) because of hypernatremia caused by pure
water loss in the kidneys
Most pts compensate for fluid loss by drinking large amounts
of water so that serum osmolality remains normal or is
moderately elevated
Pt may be fatigued from Nocturia and experience generalized
weakness
Onset of central DI is usually acute and accompanied by
excessive fluid loss.
After intracranial surgery central DI has a trihasic pattern:
the acute with an abrupt onset of polyuria, an interphase in
which urine volume normalizes and a THIRD phase in which
central DI is permanent
The third phase occurs within 10-14 days post op
Central DI from head trauma is tx well when underlying
cause is tx
DI following cranial surgery is most likely to be
permanent
Even though s/s of nephrogenic are similar to those of
central DI are similar the onset and amount of fluid
loss is less dramatic
If oral fluid intake cannot keep up with urinary losses
severe dehydration results
Manifested by poor tissue turgor, hypotension,
tachycardia, and hypovolemic shock
In addition pt may show CNS manifestations from
irritability and mental dullness to coma, related to
increasing serum osmolality and hypernatremia
Diagnostic studies
Pts with DI excrete dilute urine at a rate greater than
200 mL/hr with a specific gravity less than 1.005
Identification of central DI requires a WATER
DIPREVATION TEST
Before the test body weight, and urine
osmolality, volume, and specific gravity is
measured
The pt is deprived of water for 8-12 hours, and
then given desmopressin acetate (DDAVP) subQ or
nasally
Pts with central DI exhibits a dramatic increase in
urine osmolality from 100-600 mOsm/kg and a
sigfig decrease in urine volume

Pt with nephrogenic DI will not be able to increase

urine osmolality to greater than 300 mOsm/kg
Another test to differentiate central DI from nephrogenic
DI is to measure the level of ADH after an analog of ADH
(demopressin) is given
If cause is central kidneys will respond to
hormone by concentrating the urine
If kidneys DO NOT respond then the cause is
nephrogenic
o Nursing and Collaborative Care
Early detection, maintenance of adequate hydration,
and pt teaching for long term management
Therapeutic goal maintain fluid and electrolyte
balance
For central DI fluid and hormone replacement
In acute DI IV hypotonic saline or dextrose 5% in
water is given and titrated to replace urine output
IV glucose solutions are used monitor serum
glucose levels b/c hyperglycemia and glycosuria
can lead to osmotic diuresis which increases the
fluid volume deficit
Monitor BP, HR, and urine output and specific
gravity is essential and may be required hourly in
pts who are acutely ill
Monitor LOC for signs of acute dehydration by
assessing alertness, response to stimuli, mucous
membranes, tachycardia, and skin turgor
Maintain accurate I&Os
Daily weights
Determine fluid volume status
DDVAP, an analog of ADH, hormone replacement of
choice for central DI
Other ADH replacement drugs Vasopressin (Pitressin)
or lysine vasopressin (Diapid)
Assess response of DDAVP weight gain, H/A,
depression, restlessness, and hyponatremia
Monitor pulse, BP, LOC, I&Os, and urine specific
gravity
Chlorpropramide (Diabinese) and carbamazepine
(Tegretol) are used to help decrease thirst
associated with central DI
b/c kidney is unable to respond to ADH in nephrogenic
DI, hormone therapy has little effect

INSTEAD TX dietary measures (low-sodium diet)

and thiazide diuretics (hydrochlorothiazide
[hydroDiuril], chlorothiazide [Diuril], which may
reduce flow to the ADH- sensitive distal nephrons
Limiting sodium intake less than 3g/day to help
decrease urine output
When low sodium diet AND thiazide drugs are not
effective Indomethacin (Indocin) NSAID that
helps increase responsiveness to ADH

Disorder of Thyroid Gland

Thyroid hormones like T4 and T3 regulate energy metabolism and
growth and development
Disorders of the thyroid gland include goiter, benign and malignant
nodules, inflammation, hyperthyroidism, and hypothyroidism
Goiter
Is an enlarged thyroid gland
In a person with goiter the thyroid cells are stimulated to grow
which may result in an hyperthyroidism and hypothyroidism
MOST COMMON CAUSE WORLDWIDE OF GOITER iodine
deficiency esp in diet
In the United states the most common cause goiter is most
often due to the overproduction or underproduction of thyroid
hormones or to nodules that develop in the gland itself
Goitrogens food or drugs that contain thyroid-inhibiting
substances can cause goiter
Nontoxic goiter diffuse enlargement of the thyroid gland that
does NOT result from malignancy or inflammatory processes
o Normal levels of thyroid hormone are associated with this
type of goiter

Nodular goiter thyroid secreting nodules that function

independent of TSH stimulation
o There may be multiple nodules or single
o Usually benign follicular adenomas
o if these nodules are associated with hyperthyroidism =
toxic nodular goiters
Toxic Nodular Goiters commonly found in pts with Graves
disease
o Equally affects men and women
o Frequency of reoccurrence is 40 yrs of age
Table 50-4 Goitrogens
Thyroid Inhibitors
Foods
Other Drugs
Propylthiouracil (PTU) Broccoli
Sulfonamides
Methimazole
Brussels Sprouts
Salicylates
(Tapazole)
Iodine in large
Cabbage, cauliflower, P- Amniosalicyclic acid
amounts
Kale
Mustard, panuts,
Lithium
turnips
and amiodarone
(cordarone)

In a person with goiter, TSH and T4 levels are measured to

determine whether goiter is associated with normal thyroid
function, hyperthyroidism or hypothyroidism
Thyroid antibodies (thyroid peroxidase [TPO] antibodies) are
measured to assess for thyroiditis
Tx with thyroid hormone may prevent further enlargement
Surgery is used to remove large goiters
Goiter is a manifestation of thyroid disorders

Thyroiditis
Inflammation of the thyroid gland frequent cause of goiter
Subacute Granulomatous thyroiditis caused by viral infection
usually
Acute thyroiditis due to bacterial or fungal infection
Subacute and acute forms of thyroiditis are abrupt onset
Pt complains of pain localized in the thyroid or radiating to the
throat, ears, or jaw
Other systemic manifestations include fever, chills, sweats, and
fatigue
Hashimotosthyroiditis(chronicautoimmunethyroiditis)resultsin

hypothyroidismcausedbythedestructionofthyroidtissuebyantibodies.
o Mostcommon.

o Factorsplacinganindividualathigherriskincludefemalegender,a

positivefamilyhistory,olderage,andwhiteethnicity.
o Thegoiter,whichisthehallmarkofHashimotosthyroiditis,may
developgraduallyorrapidly.
o Ifthethyroidglandenlargesrapidly,structuresintheneck(e.g.,
tracheaandlaryngealnerves)maybecomecompressed,thus
changingthevoiceandaffectingbreathing.
Silent,painlessthyroiditis,whichmaybeearlyHashimotosthyroiditis,can
occurinpostpartumwomen.
o Thiscondition,whichisusuallyseeninthefirst6monthsafter
delivery.
o maybeduetoanautoimmunereactiontofetalcellsinthemothers
thyroidgland.
T4andT3levelsareinitiallyelevatedinsubacute,acute,andsilent
thyroiditisbutbecomedepressedwithtime.
InchronicHashimotosthyroiditis,thyroidhormonelevelsareusuallylow
andtheTSHlevelishigh.
Suppressionofradioactiveiodineuptake(RAIU)isseeninsubacuteand
silentthyroiditis.
AntithyroidantibodiesarepresentinHashimotosthyroiditis.
Recoveryfromacuteorsubacutethyroiditismaybecompleteinweeksor
monthswithoutanytreatment.
Ifthethyroiditisisbacterialinorigin,treatmentmayincludespecific
antibioticsorsurgicaldrainage.
Inthesubacuteandacuteforms,NSAIDs(aspirinornaproxen[Aleve])are
usedtorelievesymptoms.
Withmoreseverepain,corticosteroids(e.g.,prednisoneupto40mg/day)
areusedtorelievediscomfort.
o Thistreatmentmayberequiredforseveralmonthsandthenshould
bewithdrawngradually.
Propranolol(Inderal)oratenolol(Tenormin)maybeusedtotreatthe
cardiovascularsymptomsrelatedtoahyperthyroidcondition.
Thyroidhormonetherapyisindicatedifthepatientishypothyroid.
Nursingcareofthepatientwiththyroiditisincludespatientteaching
regardingthediseaseprocessandcourseoftreatment.
o Stresstheimportanceofnotabruptlydiscontinuingmedications.
o Instructthepatienttoremainunderclosehealthcaresupervisionso
thatprogresscanbemonitored.
o Teachthepatienttoreporttothehealthcareprovideranychangein
symptoms,suchasdifficultybreathingorswallowing,swellingto

faceandextremities,orrapidweightgainorloss.
o ThepatientwithHashimotosthyroiditisisatriskforother

autoimmunediseasessuchasAddisonsdisease,perniciousanemia,
orGravesdisease.
o Teachthepatientthesignsandsymptomsofthesedisorders,
particularlyAddisonsdisease.
o Instructthepatientreceivingthyroidhormoneabouttheexpected
sideeffectsofthesedrugsandmeasurestomanagethem.

Thyroid Dysfunction

Hyperthyroidism

Assessment
Lethargy and fatigue

Typical manifestations of hypothyroidism

Weakness, muscle aches, paresthesias
Intolerance to cold
Weight gain
Dry skin and hair
Loss of body hair
Bradycardia
Constipation
Generalized puffiness and edema around the eyes and face.
Forgetfulness and loss of memory
Menstrual disturbances
Cardiac enlargement, tendency to develop congestive heart failure.
Complications
Myxedema coma, the most severe form of hypothyroidism, is rare. It
may be caused by an infection, illness, exposure to cold, or certain

medications in people with untreated hypothyroidism. Signs and

symptoms of myxedema coma are:
Below normal temperature
Decreased breathing
Low blood pressure
Low blood sugar
Unresponsiveness
Gerontologic Considerations
The higher prevalence of hypothyroidism in the elderly population may
be related to alterations in immune function with age. Depression,
apathy, or decreased mobility or activity may be the major initial
symptom. In all patients with hypothyroidism, the effects of analgesic
agents, sedatives, and anesthetic agents are prolonged; special
caution is necessary in administering these agents to elderly patients
because of concurrent changes in liver and renal function. Thyroid
hormone replacement must be started with low doses and gradually
increased to prevent serious cardiovascular and neurologic side
effects, such as angina. Regular testing of serum TSH is recommended
for people older than 60 years. Myxedema and myxedema coma
generally occur in patients older than 50 years.
Diagnostic Evaluation
Thyroid-stimulating hormone (TSH) assay result is >4.0 mU/L ( normal
values: 0.51.5 mU/L). Normal value excludes primary hypothyroidism
and a markedly elevated value confirms the diagnosis.
Thyroxine (T4) radioimmunoassay decreased (normal values: 5.012.0
g/dL). Reflects underproduction of thyroid hormones; monitors
response to therapy.
Tri-iodothyronine (T3) radioimmunoassay decreased (normal values:
80230 ng/dL). Reflects underproduction of thyroid hormones.
Electrocardiogram (ECG) reveals low voltage, T wave abnormalities.
Other Tests: 24-hr radioactive iodine uptake; thyroid autoantibodies;
antithyroglobulin

Nursing Diagnosis
Activity Intolerance related to weakness and apathy
Medical Management

The primary objective is to restore a normal metabolic state by

replacing thyroid hormone. Additional treatment in severe
hypothyroidism consists of maintaining vital functions, monitoring ABG
values, and administering fluids cautiously because of the danger of
water intoxication.
Most patients are diagnosed and treated on an outpatient basis. The
goal of treatment is to return the patient to the euthyroid (normal)
state and to prevent complications. The treatment of choice is to
provide thyroid hormone supplements to correct hormonal deficiencies.
Treatment of the elderly patient is approached more cautiously
because of higher risk for cardiac complications and toxic effects. The
medication should not be given if the pulse rate is greater than 100.
The treatment is considered to be life-long, requiring ongoing medical
assessment of thyroid function.
Polypharmacy is a significant concern for the hypothyroid patient.
Several classifications of drugs are affected by the addition of thyroid
supplements, including beta blockers, oral anticoagulants,
bronchodilators, digitalis preparations, tricyclic antidepressants, and
cholesterol lowering agents.
Because significant cardiovascular disease often accompanies
hypothyroidism, the patient is at risk for cardiac complications if the
metabolic rate is increased too quickly. Therefore, the patient needs to
be monitored for cardiovascular compromise (palpitations, chest pain,
shortness of breath, rapid heart rate) during early thyroid therapy. The
diet for the hypothyroid patient is generally low in calories, high in
fiber, and high in protein. As the metabolic rate rises, the caloric
content can be increased. The patients intolerance to cold may extend
to cold foods,making meal planning more difficult.
Pharmacologic Highlights
Treatment consists of replacing the deficient hormone with synthetic
thyroid hormone; low doses are initially used, and the dose is increased
every 1 to 2 months based on the clinical response and serial
laboratory measurements that show normalization of thyroidstimulating hormone (TSH) levels in primary hypothyroidism. The
patient begins to experience clinical benefits in 3 to 5 days, which level
off after approximately 4 to 6 weeks. After the dose is stabilized,
patients can be monitored with laboratory measurement of TSH
annually.
Levothyroxine sodium a synthetic thyroid hormone replacement is
used to returns the patient to the euthyroid (normal) state. Dosage is
1.52.5 mcg/kg PO daily; (use lowest dose possible because overreplacement of thyroid can cause bone loss or cardiovascular
complications).
Nursing Management
Promoting Home and Community-Based Care

TEACHING SELF-CARE
Oral and written instructions should be provided regarding the
following:
Desired actions and side effects of medications
Correct medication administration
Importance of continuing to take the medications as prescribed even
after symptoms improve
When to seek medical attention
Importance of nutrition and diet to promote weight loss and normal
bowel patterns
Importance of periodic follow-up testing
CONTINUING CARE
Monitor the patients recovery and ability to cope with the recent
changes, along with the patients physical and cognitive status and the
patients and familys understanding of the instructions provided
before hospital discharge.
Document and report to the patients primary health care provider
subtle signs and symptoms that may indicate either inadequate or
excessive thyroid hormone.
Documentation Guidelines
Physical findings: Cardiovascular status, bowel activity, edema,
condition of skin, and activity tolerance
Response to medications, skin care regimen, nutrition

Psychosocial response to changes in bodily function, including mental

acuity
Discharge and Home Healthcare Guidelines
Explain all medications, including dosage, potential side effects, and
drug interactions.
Instruct the patient to check the pulse at least twice a week and to
stop the thyroid supplement and notify the physician if the pulse is
greater than 100.
Explain that the healthcare professional should be notified about the
condition.
Explain that ongoing medical assessment is required to check thyroid
function and that the medications may lead to hyperthyroidism despite
the patients underlying hypothyroidism.
Teach the patient about the thyroid gland and hypothyroidism, as well
as complications such as heart disease and edema.
Teach the patient that new cardiac or hyperthyroidism symptoms need
to be reported immediately.
Explain that the caloric and fiber requirements vary.
The patient should report any abnormal weight gain or loss or change
in bowel elimination.
Hyperparathyroidism

Disorders of Adrenal Cortex

Cushings Syndrome

Addisons Disease

*Use Nurse Labs, Mike, and ATI