The Endocrine

System

Plays vital role in

orchestrating
cellular
interactions,
metabolism,
growth,
reproduction,
aging, and
response to
adverse conditions

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Hormones
• Chemical transmitters released throughout the
endocrine system
• Regulate and integrate body functions
• Most are produced by endocrine glands and released
directly into bloodstream
• Others released via exocrine glands: sweat glands, GI
tract.
• Hormone concentration in the bloodstream is
maintained at a constant level.
• Negative Feedback Mechanism: To prevent
accumulation, their production
Spring 2025 is inhibited until the 2
Diagnostic Workup for Endocrine
Disorders
• Health history
• Physical Assessment
• Blood levels of circulating hormones
• Blood levels of autoantibodies
• Urine tests
• Imaging studies-MRI, CT Scan, X-rays
• Genetic screening

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Hypothalamus
• Primary controller of Endocrine System
• Regulates function of anterior pituitary
• Produces ADH (vasopressin) & Oxytocin
• Stimulates adrenal medulla to secrete epinephrine &
norepinephrine
• Monitors homeostasis

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Pituitary Gland

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Pituitary Gland or
Hypophysis
1. Attached to inferior portion
of brain.
2. Connected to
hypothalamus.
3. 2 Lobes-anterior and
posterior
4. Known as master gland
of body
5. Alterations in function r/t
problems in the gland,
tumor, trauma, radiation of
head/neck or hypothalamic
dysfunction. Spring 2025 6
Anterior Pituitary
Hormones
• Growth Hormone (GH)
• Thyroid Stimulating Hormone (TSH)
• Adrenocorticotropic Hormone (ACTH)
• Follicle-Stimulating Hormone (FSH)
• Luteinizing Hormone (LH)
• Melanocyte-Stimulating Hormone (MSH)
• Prolactin (PRL)

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 Posterior/Hypo Posterior/Hyper
Diabetes Insipidus-rare disorder, Syndrome of inappropriate
deficiency of ADH. antidiuretic hormone (SIADH). Excess
ADH.
Main cause is head trauma
Causes-head trauma, certain cancers,
Symptoms: tumors, infection of the brain.
• Urine output>250mL/hr Symptoms:
• Dilute • Pt. retains fluids
• Sp. Gravity 1.001-1.005 • Dilutional hyponatremia.
• Intense thirst • Treatment aimed at underlying
• Can develop acutely or slowly cause.
• Desmopressin orally or intranasally. • Usually self-limiting.
Causes vasoconstriction. Caution in • Fluid restriction.
cardiac patients. Take in the evening.
Blow nose gently prior to taking • Furosemide
intranasally. Dose will be increasedNursing Management:
until no nocturia.
Strict I/O
Daily weight
Urine/Blood
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Pituitary Tumors Manifestations
• Most slow growing and benign
• Can secrete hormones or not
• Symptoms are from the pressure exerted by the growing tumor in the
brain (visual disturbances, headache), from the endocrine dysfunction or
from effects on target organs.
• Tumors can grow from different types of cells resulting in different
symptoms:
• Basophilic tumors cause Cushing’s syndrome
• Eosinophilic tumors excretes excess GH. If it grows in childhood, it
causes gigantism.
In early adults it causes acromegaly an enlargement of
peripheral body parts and soft tissue.
• Chromo-phobic tumors-occur 90% of time
Produce no hormones
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Acromegaly Gigantism

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Hypophysectomy-surgically, irradiation, cryosurgery
Pre-op Nursing Intervention: Evaluation of LOC, identify
neurological deficits.
Post-op Nursing Intervention: Depends on surgical approach
Below the hairline-Maintain head of bed elevated @ 30 degrees with neck is a neutral position. Position pt. on back or non-
operated side
Nape of neck-Keep neck straight, avoid neck flexion. Position on either side.
Upper lip-Maintain nasal packing. Avoid having pt. blow nose, oral care as per facility, head of bed elevated to promote
venous drainage and drainage from surgical site.
Replacement hormone therapy will be needed.

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Thyroid Gland-the largest
endocrine organ
Controls cellular metabolic activity

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 Thyroid Hormones
• Iodine is required for normal thyroid function
• Thyroid releasing hormone (TRH) from the hypothalmus, controls
the release of TSH
• TSH from the anterior pituitary controls the release of thyroid
hormones.
• If thyroid hormone concentration decreases, the release of TSH
increases as well as the reverse situation.
• 3 hormones: T3 triiodothyronine, T4 thyroxine & calcitonin
• T3 is more potent and rapid-acting than T4
• Calcitonin is secreted in response to high plasma calcium leve. It
reduces the plasma level by increasing calcium deposit in bones.
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Thyroid Diagnostic Evaluation
• Physical Assessment- • Fine-needle biopsy
especially inspection,
palpation of lower neck. • Thyroid scans
• TSH-primary screening test • Serum thyroglobulin
• Serum-free T4 • Ask about other meds,
ingestion of kelp and seaweed
• T3 – 80-200 ng/dL as iodine metabolism can be
• T4 -5-12 mug/dL affected.
• Thyroid antibodies
• Radioactive iodine uptake-
contraindicated if allergic to
iodine/shellfish

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Hypothyro
id
Causes
95% deficiency of thyroid gland function, auto-immune
thyroiditis(Hashimoto), thyroidectomy, anti-thyroid meds

Symptoms
Fatigue, lethargy, weight gain, cold intolerance, peripheral
edema of hand and feet, dry skin.
If long standing/older adult: bradycardia, conduction
abnormalities.

Severe hypothyroidism
Low body temp, bradycardia, hair thins and falls out, face b/c
expressionless and masklike, mental processes dull, quiet and
subdued, personality changes.Spring 2025 17
Diagnostic
Results
• Physical Assessment especially of the neck. Thyroid
may be enlarged

• TSH will be increased

• T3, T4 decreased

• Decrease in radioactive iodine uptake

• Increased levels of thyroid antibodies

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Interventi
ons
Life-long hormone replacement

Medications-
• Synthetic Levothyroxine (T4)-med of choice. Titrated
until TSH is optimum level. Taken in AM.

• Patient Education-medication interactions (warfarin,

bronchodilators, vasopressors, insulin, estrogen,
sedatives)

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 Complications of Hypothyroidism

Myxedema Coma- rare life-threatening condition.

Causes-undiagnosed hypothyroidism, non-compliance w/thyroid

med

S/S-Hypothermic, unconscious, bradypnea, bradycardia.

Untreated patient goes into shock.
40% mortality

Treatment-hormone replacement
Supportive care - ABCs

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Hyperthyroid

Causes
Grave’s Disease (an autoimmune disorder), toxic multinodular
goiter, thyroiditis, excess of thyroid med.

Symptoms
Anxious, restless, irritable
May have fine tremors of hands. Tachycardic, arrhythmias
Increased appetite, muscle wasting, weight loss, sweating,
heat intolerance,
Exophthalmos (patients with Grave’s Disease) abnormal
protrusion of eyes. May have decreased blinking, lid retraction.

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Diagnostic
Results
Physical Assessment of the neck reveals gland is enlarged and
soft, may have a thrill and bruit.

Decreased serum TSH

Increased T4

Increase in radioactive iodine uptake

Increased levels of thyroid antibodies

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Medical Mgt. -depends on underlying cause.

Grave’s Disease-radioactive iodine* >80% successful

Beta adrenergic blocking meds-atenolol, propranolol,

metoprolol

Anti-thyroid med-thionamides

Surgery

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Complication of Hyperthyroidism

Thyroid Storm (Thyrotoxic Crisis)- usually abrupt onset

Uncommon today b/c improved diagnosis/treatment

Causes-thyroid surgery, radioactive iodine treatment (thyroid

gland initially increases the release of thyroid hormones), major
physical stress, not taking anti-thyroid meds, pregnancy, extreme
emotional stress.

S/S
Hyperpyrexia > 101.3º
Tachycardia >130/min
Altered neuro/mental state
May have-diarrhea, abdominal pain, weight loss,
chest pain, dyspnea, palpitations.
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 Treatment-focused on reducing body temp and
heart rate
to prevent vascular collapse.
ABCs

Hypothermia mattress/blanket, ice packs, cool environment

Acetaminophen
ASA contraindicated as it displaces thyroid hormone and
Increases hypermetabolism.

IV Fluids w/dextrose

Propylthiouracil or methimazole-decreases formation of

thyroid hormones

Hydrocortisone to treat shock & adrenal insufficiency

Iodine to decrease output of T4

Propranolol, digoxin to reduce cardiac symptoms

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Surgical management – reserved for pregnant patients, pts with large
goiters or who are unable to take antithyroid meds or patients who require
rapid normalization.
Thyroidectomy (5/6 lobes are removed)
Patient is given antithyroid med until signs of hyperthyroidism stop. Effort made to spare parathyroid
tissue to prevent hypocalcemia post op.

Post-op:

ABCs

Tracheostomy, suction, O2 is kept at bedside

Assess for laryngeal nerve damage. Have patient speak as little as possible but note voice changes.

Monitor vital signs for indications of internal

bleeding.

Assess for difficulty breathing which can be edema

of epiglottis or hematoma formation.

Head should be supported when turning.

Semi-Fowlers with the head elevated and supported
by pillows. Spring 2025 26
Hypocalcemia can
occur with injury to
parathyroid gland.
Signs/Symptoms - facial twitching,
spasms of hands/feet.
Chvostek’s & Trousseau signs
Can cause laryngospasm
Serum calcium <9

Treatment- IV Calcium gluconate.

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Parathyroid Glands – four glands on the posterior thyroid

Parathormone regulates
calcium and phosphorus
balance

Increased parathormone
elevates blood calcium by
increasing calcium
absorption from the kidney,
intestine, and bone.

Parathormone lowers
phosphorus level. Spring 2025 28
Hyperparathyroidism
• Incidence: Primary hyperparathyroidism occurs
two to four times more often in women
• Manifestations: the patient may have no
symptoms or may experience signs and
symptoms resulting from involvement of
several body systems. Apathy, fatigue, muscle
weakness, nausea, vomiting, constipation,
hypertension, and cardiac dysrhythmias may
occur
• Treatment: surgical removal of abnormal
parathyroid tissue, hydration therapy

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Hypoparathyroidism
Lack of parathormone results in decreased absorption of calcium from
the GI tract and decreased reabsorption of calcium from bone and the
kidneys. When Ca decreases, kidneys hold on to phosphate
• Causes:
• Abnormal parathyroid development
• Destruction of the parathyroid glands (surgical removal or
autoimmune response)
• Vitamin D deficiency
• Most common, near total removal of thyroid gland*
• Clinical manifestations:
• Tetany, numbness, tingling in extremities, stiffness of hands and
feet, bronchospasm, laryngeal spasm, carpopedal spasm, anxiety,
irritability, depression, delirium, ECG changes
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Tetany, Chvostek and Trousseau Sign

• Tetany: general muscle hypertonia, with

tremor and spasmodic or uncoordinated
contractions occurring with or without efforts
to make voluntary movements
• Chvostek sign: a sharp tapping over the
facial nerve just in front of the parotid gland
and anterior to the ear causes spasm or
twitching of the mouth, nose, and eye
• Trousseau sign: carpopedal spasm is
induced by occluding the blood flow to the arm
for 3 minutes with a blood pressure cuff

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Management of Hypo-Parathyroidism

• ABCs
• Cardiac monitoring
• Increase serum calcium level to 9 to 10 mg/dL
• Calcium gluconate IV, Mg. Use w/caution in pts on digoxin,
sedatives.
• Oral calcium gluconate
• Pentobarbital to decrease neuromuscular irritability
• Parathormone may be administered; potential allergic reactions
• Quiet environment; no drafts, bright lights, or sudden movement
• Diet high in calcium and low in phosphorus
• Vitamin D
• Trach at bedside
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 Hyper-parathyroid - Increased PTH releases calcium from bones and
increases kidneys reabsorption of calcium

Causes-
Primary - overproduction of parathormone r/t benign growth.
Women>men, 60-70 years of age
Secondary-
Chronic kidney failure
Symptoms-half are asymptomatic. Symptoms are r/t body system involved and increased
Ca
Apathy, fatigue, muscle weakness, nausea, vomiting, constipation, hypertension, cardiac
arrhythmias.
Irritability to psychoses.
Nephrolithiasis
Skeletal pain and tenderness, pathologic fractures.
Increased incidence of pancreatitis, peptic ulcer

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Management of Hyperparathyroidism
Diagnostic Findings - Elevated serum calcium and parathormone
Bone changes on x-ray, bone scans
Diagnostic Tests - Ultrasound, MRI, needle biopsy
Interventions
Symptomatic - Parathyroidectomy. Minimally invasive surgery removes only
the diseased tissue.
Performed on patients with any of the following criteria: <50 yrs. old,
kidney disease, low bone density, previous fracture, nephrolithiasis.
Asymptomatic patients-monitor serum calcium levels and symptoms, organ
involvement.
Increase daily fluid intake 2000mL or more
Encourage patient to be mobile
Encourage balanced, appealing diet
Stool softeners. Spring 2025 34
Hypercalcemic Crisis - complication of
hyperparathyroidism
Occurs with extreme elevation of serum calcium levels, >13 mg/dL
Results in neurologic, cardiovascular, and kidney symptoms that
can be life threatening
Treatment:
ABCs
Rapid rehydration with large volumes of IV isotonic saline to
maintain UO 100-150mL/hr
Calcitonin to promote renal excretion of Ca and reduce bone
resorption.
Loop diuretic
Bisphosphonates to decrease serum calcium by promoting
deposit into bones and reducing GI absorption of calcium.
Dialysis in an emergency.
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Adrenals-located on each kidney. 2 parts are medulla
and cortex.

Regulated by hypothalamus and pituitary glands.

The medulla produces catecholamines (adrenaline or

epinephrine).

The cortex produces 3 types of steroid hormones:

1. Mineralocorticoid - Aldosterone regulates BP by

retaining sodium and excreting K+.

2. Glucocorticoid -Cortisol controls glucose metabolism.

3. Sex hormones - androgens

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 Glucocorticoids –regulate Mineralocorticoids-electrolyte
glucose metabolism metabolism
Increased cortisol=increased They effect renal tubules and GI tract.
glucose levels Cause increased sodium absorption
This is in response to the release of and potassium excretion to regulate
ACTH from the anterior pituitary. BP.
Glucocorticoids in the bloodstream, It is released when angiotensin II is
released to help constrict arterioles to
inhibit ACTH release and decreases
increase BP.
release of glucocorticoids from the
adrenal cortex.
When large amounts of oral Sex Hormones – when secreted in
steroids are used, ACTH does not normal amounts, little effect on
release glucocorticoids. Long term body.
may cause adrenals to stop In excess amounts – masculinization
functioning.
in women, femininization in men or
Abrupt withdrawal of oral steroids premature sexual development in
may cause adrenal insufficiency.
children
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 Adrenocortical Insufficiency – Addison’s
Disease
Causes - dysfunction of hypothalamus-pituitary-adrenal system
from autoimmune disorders, TB, histoplasmosis, surgical removal
of adrenals, rifampin, barbiturates, metastatic cancers. Rare.
Sudden withdrawal of exogenous steroids (PO, IV).
Signs/Symptoms- increased excretion of Na, water, Cl.
Decreased excretion of K. Causes decreased CO. (Aldosterone)
Hypoglycemia, muscle weakness, lethargy, GI symptoms
(cortisol).
Hyperpigmentation of skin
Treatment – life-long steroid replacement.

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Addisonian Crisis – life threatening complication
Signs/Symptoms – hypotension, cyanosis, fever,
nausea, vomiting, shock, confusion.
Medical Mgt – IV fluids, glucose, steroids, address N, V,
D.
Nursing Interventions – ABCs. When well patient
education about lifelong medication, how to recognize
stressors to prevent a Crisis, importance of follow-up
care.

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Cushing’s Syndrome – excess of steroids
Cause – most common is use of corticosteroid medication. Hyperplasia of the
adrenals, tumor of the pituitary, bronchogenic CA.
Signs/Symptoms - central obesity, fatty deposits in neck, back, thin legs.
Fragile skin, that bruises easily, striae. Moon-face, acne, oily skin.
Weak, disturbed sleep.
Osteoporosis, backache.
Retention of Na and water usually cause HTN, HF.
In women – btwn. 20-40 yrs., appearance of masculine traits and the resession
of feminine traits. Excessive face hair, breast atrophy, messes stop, voice
deepens, libido is lost.
Diagnostics – serum cortisol, urine cortisol, dexamethasone suppression test.
Additionally, pt. will have an increase in serum Na, glucose and a decrease in K.
Med Mgt. – For a pituitary tumor-surgery.
For adrenal hypertrophy – removal of adrenals.
For corticosteroid use – taper down to minimum dose. Spring 2025 40
 Nursing Interventions
Monitor cardiac status
Monitor F/E balance
Protective environment
Assess for infection
Promote skin integrity
Monitor for Addisonian
Crisis
Patient Education about
meds, body image, coping.

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