ENDOCRINE NURSING

Compile by
Fida Ur Rahman
RN, DPN, BScN
Nursing lecturer
 THYROID GLAND
 The thyroid gland is a butterfly-shaped organ located in the lower
neck, anterior to the trachea.
 It consists of two lateral lobes connected by an isthmus.
 This gland is about 5 cm long and 3 cm wide and weighs about 30 g.
 The blood flow to the thyroid is very high (about 5 mL/min per gram
of thyroid tissue), approximately five times the blood flow to the
liver.
 This reflects the high metabolic activity of the thyroid gland.
 The thyroid gland produces three hormones: thyroxine (T4),
triiodothyronine (T3), and calcitonin.
 THYROID HORMONES
 T4 and T3, which are referred to collectively as thyroid hormone, are
two separate hormones produced by the thyroid gland.
 Both are amino acids that contain iodine molecules bound to the amino
acid structure;
 T4 contains four iodine atoms in each molecule, and T3 contains three.
 These hormones are synthesized and stored bound to proteins in the
cells of the thyroid gland until needed for release into the bloodstream.
 About 75% of bound thyroid hormone is bound to thyroxine-binding
globulin (TBG); the remaining bound thyroid hormone is bound to
thyroid-binding prealbumin and albumin.
 FUNCTION OF THYROID HORMONES
 The primary function of thyroid hormone is to control cellular metabolic
activity.
 T4, a relatively weak hormone, maintains body metabolism in a steady state.
 T3 is about five times as potent as T4 and has a more rapid metabolic action
 These hormones accelerate metabolic processes by increasing the level of
specific enzymes that contribute to oxygen consumption and altering the
responsiveness of tissues to other hormones.
 The thyroid hormones influence cell replication and are important in brain
development.
 Thyroid hormone is also necessary for normal growth.
 The thyroid hormones, through their widespread effects on cellular metabolism,
influence every major organ system.
CALCITONIN

 Calcitonin, or thyrocalcitonin, is another important

hormone secreted by the thyroid gland.
 It is secreted in response to high plasma levels of calcium,
and it reduces the plasma level of calcium by increasing its
deposition in bone.
 GOITER
 A goiter is an enlarged thyroid gland, and it may be diffuse or nodular.
 A goiter may extend into the retrosternal space, with or without substantial
anterior enlargement.
 Because of the anatomic relationship of the thyroid gland to the trachea,
larynx, superior and inferior laryngeal nerves, and esophagus, abnormal
growth may cause a variety of compressive syndromes.
 Thyroid function may be normal (nontoxic goiter), overactive (toxic goiter),
or underactive (hypothyroid goiter).
 Initial screening for goiters should include thyroid-stimulating hormone
(TSH).
 SIGN AND SYMPTOMS
 A goiter may present in various ways, including the following:
• Incidentally, as a swelling in the neck discovered by the patient or on
routine physical examination
• A finding on imaging studies performed for a related or unrelated medical
evaluation
• Local compression causing dysphagia, dyspnea, stridor, plethora, or
hoarseness
• Pain due to hemorrhage, inflammation, necrosis, or malignant
transformation
• Signs and symptoms of hyperthyroidism or hypothyroidism
• Thyroid cancer with or without metastases
 INVESTIGATIONS
 Initial screening should include TSH and T3, T4S
 An assessment of free thyroxine index or direct measurement of free thyroxine
 Further laboratory testing is based on presentation and results of screening studies
and may include thyroid antibodies (antithyroid peroxidase; formerly, the
antimicrosomal antibodies and antithyroglobulin), thyroglobulin, sedimentation
rate, and calcitonin
 Ultrasonography can be used to establish and follow goiter size, consistency, and
nodularity.
 Computed tomography (CT) scanning is useful in determining the effect of the
thyroid gland on nearby structures
 Magnetic resonance imaging (MRI) has the same indications as CT scanning
 Fine-needle aspiration biopsy is employed for cytologic diagnosis OR
Core biopsy, or large-needle biopsy
 TREATMENT
 Small benign euthyroid goiters do not require treatment. The effectiveness of medical
treatment using thyroid hormone for benign goiters is controversial.
 The size of a benign euthyroid goiter may be reduced with levothyroxine suppressive
therapy. Moreover, treatment of hypothyroidism or hyperthyroidism often reduces the size
of a goiter.
 Goiters with primary thyroid malignancy require levothyroxine replacement after surgery
and radioactive iodine ablation. Metastatic lesions to the thyroid gland require treatment of
the primary malignancy. Granulomatous and infectious etiologies for goiter require specific
treatment depending on the underlying cause.
 Surgery is reserved for the following situations:
• Large goiters with compression, Malignancy or When other forms of therapy are not
practical or are ineffective
 If it is practical, treat endemic goiters in iodine-deficient regions with iodine
supplementation in the diet and avoidance of goitrogens. Treatment with iodine
 HYPOTHYROIDISM
 Hypothyroidism is a common endocrine disorder resulting from deficiency of thyroid
hormone.
 Thyroid deficiency can affect all body functions and can range from mild, subclinical
forms to myxedema, an advanced form.
 It usually is a primary process in which the thyroid gland is unable to produce
sufficient amounts of thyroid hormone.
 Hypothyroidism can also be secondary—that is, the thyroid gland itself is normal, but
it receives insufficient stimulation because of low secretion of thyrotropin (ie, thyroid-
stimulating hormone [TSH]) from the pituitary gland.
 This generally occurs in the presence of other pituitary hormone deficiencies.
 In tertiary hypothyroidism, inadequate secretion of thyrotropin-releasing hormone
(TRH) from the hypothalamus leads to insufficient release of TSH, which in turn
causes inadequate thyroid stimulation.
 ETIOLOGY
 Autoimmune disease (Hashimoto’s thyroiditis, post Graves’ disease)
 Atrophy of thyroid gland with aging
 Therapy for hyperthyroidism Radioactive iodine
 Thyroidectomy
 Medications Lithium Iodine compounds Antithyroid medications
 Radiation to head and neck for treatment of head and neck cancers, lymphoma
 Infiltrative diseases of the thyroid (amyloidosis, scleroderma, lymphoma) Iodine
deficiency and iodine excess
 More than 95% of patients with hypothyroidism have primary or thyroidal
hypothyroidism, which refers to dysfunction of the thyroid gland itself.
 If the cause of the thyroid dysfunction is failure of the pituitary gland, the
hypothalamus, or both, the hypothyroidism is known as central hypothyroidism
 PATHOPHYSIOLOGY
 Although hypothalamic or pituitary disorders can affect thyroid function, localized disease of
the thyroid gland that results in decreased thyroid hormone production is the most common
cause of hypothyroidism.
 Under normal circumstances, the thyroid releases 100-125 nmol of T4 daily and small
amounts of T3.
 The ratio of T4:T3 production varies between about 14:1 and 4:1, depending on iodine
sufficiency and TSH stimulation.
 The half-life of T4 is approximately 7-10 days, whereas the half-life of T3 is about 24 hours.
T4, a prohormone, is converted via the action of deiodinases to T3, the active form of thyroid
hormone.
 Early in the disease process, compensatory mechanisms maintain T3 levels.
 Decreased production of T4 causes an increase in the secretion of TSH by the pituitary gland.
 TSH stimulates hypertrophy and hyperplasia of the thyroid gland and 5’-deiodinase activity,
thereby increasing T3 production
 CLINICAL PRESENTATIONS
 Fatigue, loss of energy, lethargy  Forgetfulness, impaired memory,
 Weight gain inability to concentrate
 Decreased appetite  Constipation
 Cold intolerance  Menstrual disturbances, impaired
 Dry skin fertility
 Decreased perspiration
 Hair loss
 Sleepiness  Paresthesia's and nerve entrapment
syndromes
 Muscle pain, joint pain, weakness in the
 Blurred vision
extremities
 Depression  Decreased hearing
 Emotional lability, mental impairment  Fullness in the throat, hoarseness
  Pericardial effusion
 MYXEDEMA COMA
 Myxedema coma is a severe form of hypothyroidism that most
commonly occurs in individuals with undiagnosed or untreated
hypothyroidism who are subjected to an external stress. Features are
as follows:
 Altered mental status
 Hypothermia
 Bradycardia
 Hypercapnia
 Hyponatremia
 Cardiomegaly, pericardial effusion, cardiogenic shock, and ascites
may be present
 INVESTIGATIONS
 Results in patients with hypothyroidism are as follows:
 Elevated TSH with decreased T4 or FTI
 Elevated TSH (usually 4.5-10.0 mIU/L) with normal free T4 or FTI is
considered mild or subclinical hypothyroidism
 Abnormalities in the complete blood count and metabolic profile that
may be found in patients with hypothyroidism include the following:
 Anemia
 Dilutional hyponatremia (with increased antidiuretic hormone [ADH])
 Hyperlipidemia
 Reversible increases in creatinine
 MANAGEMENT
 The primary objective in the management of hypothyroidism is to restore a
normal metabolic state by replacing the missing hormone
 Synthetic levothyroxine (Synthroid or Levothroid) is the preferred
preparation for treating hypothyroidism and suppressing nontoxic goiters.
 If replacement therapy is adequate, the symptoms of myxedema disappear
and normal metabolic activity is resumed.
 Provide antibiotic coverage for sepsis
 In severe hypothyroidism and myxedema coma, management includes
maintaining vital functions.
 Arterial blood gases may be measured to determine carbon dioxide retention
and to guide the use of assisted ventilation to combat hypoventilation.
HYPERTHYROIDISM

 Hyperthyroidism presents as a constellation of symptoms

due to elevated levels of circulating thyroid hormones.
 The term hyperthyroidism refers to inappropriately
elevated thyroid function
 Hyperthyroidism is the second most prevalent endocrine
disorder, after diabetes mellitus
 GRAVES DISEASE
 Graves disease (diffuse toxic goiter), the most common form of overt
hyperthyroidism, is an autoimmune condition in which autoantibodies are directed
against the thyroid-stimulating hormone (TSH) receptor.
 As a result, the thyroid gland is inappropriately stimulated with ensuing gland
enlargement and increase of thyroid hormone production
 Thyroid storm is a rare and potentially fatal complication of hyperthyroidism.
 It typically occurs in patients with untreated or partially treated thyrotoxicosis who
experience a precipitating event such as surgery, infection, or trauma.
 Thyroid storm must be recognized and treated on clinical grounds alone, as
laboratory confirmation often cannot be obtained in a timely manner.
 Patients typically appear markedly hypermetabolic with high fevers, tachycardia,
nausea and vomiting, tremulousness, agitation, and psychosis.
 Late in the progression of disease, patients may become stuporous or comatose with
 CAUSES
 Hyperthyroidism results from numerous etiologies, including autoimmune, drug-
induced, infectious, idiopathic, iatrogenic, and malignancy.
 Autoimmune
• Graves disease
• Chronic thyroiditis (Hashimoto thyroiditis) - Although the primary cause of
hypothyroidism, the disease process occasionally presents initially with
thyrotoxicosis
• Postpartum thyroiditis - Presents similarly to subacute thyroiditis 2-6 months
postpartum but typically painless with mild symptoms
 Drug-induced
• Iodine-induced - Occurs after administration of either supplemental iodine to
those with prior iodine deficiency, amiodarone and Antineoplastic agents
 CONTI…

 Infectious
• Suppurative thyroiditis, Post viral thyroiditis
 Idiopathic
 Toxic multinodular goiter - The second most common cause of
hyperthyroidism, characterized by functionally autonomous nodules,
typically after age 50 years
 Iatrogenic
• Thyrotoxicosis factitia - A psychiatric condition in which high
quantities of exogenous thyroid hormone are consumed
 PATHOPHYSIOLOGY
 Thyroid hormone concentration is regulated by negative feedback by
circulating free hormone primarily on the anterior pituitary gland and to a
lesser extent on the hypothalamus.
 The secretion of TRH is also partially regulated by higher cortical centers.
 The thyroid gland produces the prohormone thyroxine (T4), which is
deiodinated primarily by the liver and kidneys to its active form,
triiodothyronine (T3).
 The thyroid gland also produces a small amount of T3 directly. T4 and T3 exist
in 2 forms: a free, unbound portion that is biologically active and a portion that
is protein bound to thyroid-binding globulin (TBG).
 Despite consisting of less than 0.5% of total circulating hormone, free or
unbound T4 and T3 levels best correlate with the patient's clinical status.
 CLINICAL PRESENTATIONS
 Because of the many actions of • Disorientation
thyroid hormone on various organ • Tremor
systems in the body, the spectrum of
clinical signs produced by the • Nervousness, anxiety, or emotional lability
condition is broad • Heat intolerance
• Weight loss • Increased perspiration
• Patients typically report an average • Fatigue, fever
loss of approximately 15% of their • Weakness - Typically affects proximal
prior weight. muscle groups
• Basal metabolic rate is increased with • Dehydration
a stimulation of lipolysis and
lipogenesis. • Dyspnea

• Palpitations • Frequent bowel movements

• Chest pain - Often occurs in the • Psychosis

absence of cardiovascular disease • Menstrual irregularity
 DIAGNOSIS
 Thyroid function studies confirm the diagnosis in the appropriate clinical setting.
• Elevation of free T4 and low to undetectable TSH levels are diagnostic of
thyrotoxicosis; in earlier stages, T3 rise precedes T4 rise.
• Excessive TSH levels in the setting of elevated free T4 indicate hyperthyroidism
of pituitary origin.
• Hyperglycemia
• Hypercalcemia
• Hepatic function abnormalities
• Low serum cortisol
• Leukocytosis
 Chest radiography may identify congestive heart failure or pulmonary infections,
often associated with progression to thyroid storm
 EMERGENCY TREATMENT
 Intravenous glucocorticoids are indicated if adrenal insufficiency is suspected.
 Large doses of dexamethasone (2 mg q6h) inhibit hormone production and decrease
peripheral conversion from T4 to T3.
 The warning also states that propylthiouracil should be reserved for use in those who
cannot tolerate other treatments, such as methimazole, radioactive iodine, or surgery.
 Plasmapheresis has been used successfully in medication-induced thyroid storm and in
conditions in which oral/conventional therapy is not possible.
 The patient should be intubated if profoundly altered.
 Supplemental oxygen may be required. Aggressive fluid resuscitation may be indicated.
 Fevers are treated with cooling measures and antipyretics
 Aggressive hydration of up to 3-5 L/d of crystalloid compensates for potentially
profound GI and insensible losses.
 Appropriate electrolyte replacement should be directed by laboratory values.
 NURSING DIAGNOSIS

 Based on all the assessment data, the major nursing diagnoses of the patient
with hyperthyroidism may include the following:
 Imbalanced nutrition, less than body requirements, related to exaggerated
metabolic rate, excessive appetite, and increased GI activity
 Ineffective coping related to irritability, hyperexcitability, apprehension,
and emotional instability
 Low self-esteem related to changes in appearance, excessive appetite, and
weight loss
 Altered body temperature
 NURSING MANAGEMENTS
 The appetite is increased but may be satisfied by several well-balanced meals of small size,
even up to six meals a day.
 Foods and fluids are selected to replace fluid lost through diarrhea and diaphoresis and to
control the diarrhea that results from increased peristalsis
 The patient with hyperthyroidism needs reassurance that the emotional reactions being
experienced are a result of the disorder and that with effective treatment those symptoms will
be controlled.
 The nurse conveys an understanding of the patient’s concern about these problems and
promotes use of effective coping strategies.
 The patient with hyperthyroidism frequently finds a normal room temperature too warm
because of an exaggerated metabolic rate and increased heat production. If the patient is
hospitalized, the nurse maintains the environment at a cool, comfortable temperature and
changes bedding and clothing as needed.
 The nurse closely monitors the patient with hyperthyroidism for signs and symptoms that may