UNIT 10b: SYNERGISTIC CARE OF
PATIENTS WITH ENDOCRINE
DISORDERS
NU 308: NURSING CARE OF ADULTS WITH ACUTE/COMPLEX HEALTH PROBLEMS
MARYMOUNT UNIVERSITY
SPRING 2022
OBJECTIVES
 Describe the functions of each of the endocrine glands and their hormones.
 Identify the diagnostic tests used to determine alterations in function of each of the
endocrine glands.
 Use the nursing process as a framework for care of patients with hyperthyroidism,
hypothyroidism, Cushing syndrome and Addison’s disease.
 Develop a plan of nursing care for the patient undergoing thyroidectomy.
 Compare hyperparathyroidism and hypoparathyroidism in terms of their causes, clinical
manifestations, management, and nursing interventions.
 Compare Addison disease with Cushing syndrome: their causes, clinical manifestations,
management, and nursing interventions.
 Explain nursing management of patients with adrenal insufficiency.
 Identify the education needs of patients requiring corticosteroid therapy
HypothalamicPituitary
Control
The endocrine system –
plays a vital role in
orchestrating cellular
interactions,
metabolism, growth,
reproduction, aging, and
response to adverse
conditions.
Negative feedback
mechanism
MAJOR HORMONE-SECRETING GLANDS
Organs and
Hormones
Organs
Hormones
Hypothalamus
Releasing/inhibiting
hormones
Pituitary, anterior
Tropic hormones
Pituitary, posterior
ADH, oxytocin
Thyroid
T4, T3, Calcitonin
Parathyroid
PTH
Pancreas
Glucagon/Insulin
Adrenal cortex
Cortisol, aldosterone,
androgens, estrogens
Adrenal medulla
Catecholamines
Reproductive
Estrogen/progesterone/
testosterone
TARGET
CELLS &
TARGET
ORGANS:
HORMONE
RECEPTORS
FOR EACH
SPECIFIC
HORMONE
PITUITARY
GLAND AND
HORMONES
SECRETED
ALTERATIONS
OF THE
HYPOTHALAMIC
- PITUITARY
SYSTEM
PITUITARY GLAND
 Anterior
 FSH, LH, prolactin, ACTH,
TSH, GH
 Hypersecretion: Cushing
syndrome, gigantism,
acromegaly
 Hyposecretion: dwarfism,
panhypopituitarism
 Posterior
 ADH, vasopressin
 Oxytocin
 Hyper: SIADH
 Hypo: DI
 Tumors: 95% benign
 Surgery: hypophysectomy
H
Y
P
O
P
I
T
U
I
T
A
R
I
S
M
Pituitary
Deficient
hormone
Clinical manifestations
GH
↓ bone density, fractures, ↓ muscle strength, serum
cholesterol ↑
LH, FSH
Women – amenorrhea, anovulation, ↓ estrogen levels, breast
atrophy, loss of bone density, ↓ axillary & pubic hair, ↓
libido
Men - ↓ facial hair, ↓ ejaculate vol., ↓ muscle mass, ↓
Bone density, ↓ body hair, ↓ libido, impotence
TSH
↓ Libido, wt. gain, intolerance to cold, scalp alopecia,
hirsutism, menstrual abnormalities, slow cognition, lethargy
ACTH
↓ Axillary & public hair (women), pale/sallow complexion,
malaise & lethargy, anorexia, postural hypotension,
headache, hypoglycemia, hyponatremia
ADH
(posterior)
Large ↑ urine output, ↓ specific gravity, hypovolemia, ↑
thirst & ↑ plasma osmolarity
HYPOPITUITARISM
 Hormone undersecretion
 Interventions:
 Lifelong replacement of deficient hormones
 Androgen therapy for virilization; gynecomastia
can occur
 Estrogens and progesterone
 Growth hormone
Pituitary
HYPERPITUITARISM
Causes
 Hormone oversecretion occurs with pituitary tumors or
hyperplasia
 Genetic considerations
 Pituitary adenoma
Nonsurgical management:
 Drug therapy (Parlodel, Dostinex, Permax, Sandostatin,
Somavert)
 Radiation
 Gamma knife procedure
Pituitary
HYPERPITUITARY : SURGICAL
MANAGEMENT
POSTOPERATIVE CARE
 Monitor neurologic response
 Assess for postnasal drip
 Elevate HOB
 Assess nasal drainage
 Avoid coughing soon after surgery
 Assess for meningitis
 Hormone replacement
 Avoid bending and Valsalva
 Avoid straining at stool
 Avoid tooth brushing
 Numbness in the area
of the incision
 Decreased sense of
smell
 Vasopressin
DIABETES INSIPIDUS (DI)
 Caused by injury to the hypothalamus or pituitary gland
 Water metabolism problem caused by an ADH deficiency
(either decrease in ADH synthesis or inability of
kidneys to respond to ADH)
 Classifications:
 Nephrogenic
 Neurogenic (Central)
 Psychogenic
 Drug-related
DI: PATHOGENESIS
 Deficiency of or decreased response
to ADH causing fluid loss, potentially
electrolyte disturbances
 Neurogenic, nephrogenic, psychogenic
 It results in the excretion large
amount of dilute urine ( > 250ml/hr)
 Dehydration
 Increase sodium level
CLINICAL MANIFESTATIONS &
ASSESSMENT
 Polydipsia & polyuria
 Hypo/Hypernatremia
 Low urine specific gravity
 High serum osmolarity
 Fluid volume deficit
 Weight loss
 Tenting
 Hypotension
 Tachycardia
 Shock
 Strict I & O
 Daily labs: Na
 Collect urine sample
 Collect serum osmolality per MD
order
 Assessment:
 Daily weight
 Vital signs
 Skin turgor
NURSING CARE: D.I.
 Assessment of fluid volume status
 I & O, daily weights, urine output
 Medication administration
 DDAVP: increase dose if urine output increases while specific gravity is low
 Teaching:
 Med administration: DDAVP
 HA, nausea, vomiting, signs of hyponatremia, seizures
 Home maintenance
 Daily weight
 Regular blood work
SIADH
 Vasopressin secreted even when plasma osmolarity is low or normal
 Feedback mechanisms do not function properly
 Water is retained, results in hyponatremia (decreased serum
sodium level)
 Findings:
 Recent head trauma
 Cerebrovascular disease
 TB or other pulmonary disease
 Cancer
 All past and current drug use
 Decrease in serum sodium levels
SIADH: PATHOGENESIS
 ↑ ADH  ↑ water
reabsorption in kidneys
 Dilutional hyponatremia
 ↑ water retention without
peripheral edema
 ↓ renin & aldosterone
CLINICAL MANIFESTATIONS
 Most manifestations are due to hypotonic (dilutional) hyponatremia;
extent determined by severity and rapidity of onset of
hyponatremia
 Rapid ↓ in NA from 140-130 mEq/L
 ↑ BP, thirst, impaired taste, anorexia, dyspnea on exertion, fatigue, dulled
sensorium; usually no peripheral edema.
 Na ↓ from 130-120 mEq/L
 Severe vomiting and abdominal cramps
 Na < 115 mEq/L
 Confusion, lethargy, muscle twitching, convulsions
 Na below 110-115 mEq/L can cause severe, sometimes irreversible, neurologic damage
ANTIDIURETIC HORMONE ANTAGONIST
(VASOPRESSIN ANTAGONISTS)
 Conivaptan (Vaprisol)
 ADH antagonist
 Used in short-term IV therapy for hyponatremia in hospitalized patients with
euvolemia and/or hypervolemia
 Monitor serum sodium closely owing to risk of hypernatremia
 Tolvaptan
 Oral vasopressin antagonist
 Used to reduce hyponatremia in euvolemic or hypervolemic patients
SIADH INTERVENTIONS
 Fluid restriction (500-1000 cc/day)
 Drug therapy (diuretics, hypertonic saline, demeclocycline,
Vasopressin antagonists)
 Monitor for fluid overload
 Safe environment
 Neurologic assessment
SIADH
CARE & MANAGEMENT
**Treat underlying cause!**
Mild hyponatremia: restrict fluids to 800-1000 cc/day to increase serum Na &
serum osmolality
Severe hyponatremia: hypertonic NSS administered (3%-5%) slowly plus fluid
restriction of 500 cc daily
Note: Be careful when correcting hyponatremia – rapid rise in sodium levels may
cause brain damage!
++ Remove meds causing excess ADH++
NURSING MANAGEMENT: ACUTE
 Identify chronic SIADH pts or those at high risk
 Urine output < 30 cc/hr
 Daily weights (no edema)
 Daily labwork: Na+, osmolality
 Assess fluid overload
NURSING MANAGEMENT: CHRONIC
 Adheres to fluid restriction
 800-1000 cc daily
 Maintains follow-up appointments
 Blood work
 Medication compliance
 Diuretics
 Electrolyte replacement
 Teaching
 When to call MD: electrolyte imbalance
 Meds (take with meals)
SIADH VS DI
Disorder
SIADH
Dehydration
Diabetes
Insipidus
Serum
Na+
Serum
Osmolality
Urine
Osmolality
THYROID
 Thyroid hormones: T3, T4,
calcitonin
 Iodine is contained in thyroid
hormone
 TSH from the anterior
pituitary controls the release
of thyroid hormone
 Controls cellular metabolic
activity
 T3 is more potent and rapid-
acting than T4
 Calcitonin is secreted in
response to high plasma
calcium level and increases
calcium deposit in bone
HYPOTHALAMIC–PITUITARY–THYROID AXIS
THYROID
FEEDBACK
THYROID DIAGNOSTIC TESTS
 TSH
 Fine-needle biopsy
 Serum-free T4
 Thyroid scan, radioscan, or
 T3 and T4
 T3 resin uptake
 Thyroid antibodies
 Radioactive iodine uptake
scintiscan
 Serum thyroglobulin
THYROID FUNCTION TESTS
 Serum thyroid-stimulating hormone (TSH)
 Screening and diagnosis of hypothyroidism
 Elevated TSH is indication of hypothyroidism
 Serum T4 test
 Can measure total T4 or free T4
 Serum T3 test
 Can measure total T3 or free T3
GOITER
 Defined as an enlargement of the thyroid gland
that is also characterized by hypertrophy of
the gland
 Causes:
 Excess TSH stimulation
 Lack of circulating thyroid hormones
 Thyroiditis
THYROID DISORDERS
 Cretinism
 Hyperthyroidism
 Hypothyroidism
 Thyroiditis
 Goiter
 Thyroid cancer
HYPERTHYROIDISM
 Graves’ disease (most common cause);
thyrotoxicosis: excessive output of
thyroid hormone (thyroid storm)
 Autoimmune disorder
 Affects women eight times more than
men
 Clinical manifestations
 Nervousness; rapid pulse; heat intolerance;
tremors; skin flushed, warm, soft, and moist;
exophthalmos; increased appetite; weight loss;
elevated systolic BP; cardiac dysrhythmias
thyroid
THYROTOXICOSIS (GRAVES DISEASE)
CLINICAL MANIFESTATIONS:
GRAVES DISEASE
thyroid
 Arrhythmias
 Goiter
 Angina
 Intolerance to heat
 Fatigue
 Menstrual irregularities
 Insomnia
 Exophthalmos
 Weight loss *
 Nervousness *
 Increased appetite
 Diarrhea
 Diaphoresis
*early symptoms
HYPERTHYROIDISM
MEDICAL MANAGEMENT OF
HYPERTHYROIDISM
 Radioactive 131I therapy – one single dose effective in most cases
 Iodine therapy- thyroid tissue specific
 Medications- anti thyroids medications (lots of side effects)
 Surgery; subtotal thyroidectomy
PHARMACOLOGIC AGENTS USED TO TREAT
HYPERTHYROIDISM
THYROID STORM: THYROTOXIC CRISIS
 AKA: Thyroid Storm
 Interventions:
 Heightened state of hyperthyroidism
 Adequate O2/ airway
 Assess:
 Control dysrhythmias/IVF/
 Nausea & Vomiting
 Severe tachycardia
 Heart failure
 Delirium
 Hyperthermia
 Shock & coma
anti-thyroid drugs
 Calm, quiet environment =
reduced stress
 Cool room with light covers
THYROIDITIS
 Inflammation of thyroid gland
 Three types—acute; subacute (granulomatous); chronic
(Hashimoto’s disease—most common type)
 Thyroiditis vs. hyperthyroidism, hypothyroidism
 Nonsurgical management, drug therapy
 Surgical management
thyroid
THYROID CANCER
 Four types:
 Papillary
 Follicular
 Medullary
 Anaplastic
 Collaborative management
 Surgery
THYROIDECTOMY
 Treatment of choice for thyroid cancer
 Modified or radical neck dissection, possible radioactive iodine to
minimize metastasis
 Preoperative goals: reduction of stress and anxiety to avoid precipitation
of thyroid storm
 Preoperative education: dietary guidance to meet patient’s metabolic
needs, avoidance of caffeinated beverages and other stimulants,
explanation of tests and procedures, and head and neck support used
after surgery
POSTOPERATIVE CARE
 Monitor respirations; potential airway impairment
 Emergency tracheotomy tray at bedside
 Monitor for potential bleeding and hematoma
formation; check posterior dressing
 Assess pain and provide pain relief measures
 Semi-Fowler position, support head and neck
 Assess voice, discourage talking
 Potential hypocalcaemia related to injury or removal of
parathyroid glands; refer to Chart 52-6
HYPOTHYROIDISM
 Insufficient circulating thyroid
hormone
 Primary vs. secondary causes
 Thyroid destroyed, decreased (primary)
 Decreased TRH or TSH (secondary)
 Male = Female
 All ages
thyroid
HYPOTHYROIDISM ASSESSMENT
 History
 Physical assessment
 Clinical manifestations
 Psychosocial assessment
 Laboratory assessment
CLINICAL MANIFESTATIONS
 Slowing of normal body








processes
Personality changes
Fatigue
Lethargy
Mental changes: impaired
memory & slow speech
Downtrodden appearance
Intolerance to cold
Hair loss
Dry & coarse skin
 Brittle nails
 Muscle weakness & swelling
 Constipation due to decreased GI






motility
Weight gain
Menorrhagia
Decreased CO and contractility =
DOE
Anemia
Increased Bruising
Increased cholesterol
HYPOTHYROIDISM
MYXEDEMA
CARE & MANAGEMENT: HYPOTHYROIDISM
 Teaching:
 Medication compliance
 Follow-up: MD appointments, blood work
 Signs & symptoms of hyper/hypothyroidism
 Overdose: orthopnea, dyspnea, tachycardia, palpitations, nervous, insomnia
 DM patients: glucose elevation once euthyroid state achieved
HYPOTHYROID DRUGS
 Levothyroxine (Synthroid)
 Synthetic preparation of thyroxine (T4) and drug of choice for
hypothyroidism
 Conversion to T3
 Half-life: 7 days
 Used for all forms of hypothyroidism
 Should be taken in the morning at least 30 to 60 minutes before breakfast
 Adverse effects
 Tachycardia
 Angina
 Tremors
 Can intensify effects of warfarin
HYPOTHYROID DRUGS
 Levothyroxine (Synthroid)
 Drug interactions
 Drugs that reduce levothyroxine absorption
 Drugs that accelerate levothyroxine metabolism
 Warfarin
 Catecholamines