Assessment and Management

of Patients With Endocrine

Disorders
Anatomic and Physiologic Overview
• release of chemical transmitter substances known as hormones
•  Effects almost every cell, organ, and function of the body
• The endocrine system is closely linked with the nervous system and
the immune system
• Negative feedback mechanism
• Chemical messengers of the body
• Act on specific target cells
Classification of Hormones
• amines and amino acids
• (e.g., epinephrine, norepinephrine, and thyroid hormones);
• peptides, polypeptides, proteins, and glycoproteins
• (e.g., thyrotropin-releasing hormone [TRH], follicle-stimulating hormone
[FSH], and growth hormone [GH]);
• Steroids
• (e.g., corticosteroids, which are hormones produced by the adrenal cortex or
their synthetic equivalents); and
• fatty acid derivatives
• (e.g., eicosanoid, retinoids)
Health History

• Assessment of changes in:

• energy level, • menstrual cycle,
• tolerance to heat or cold, • memory,
• weight, thirst, • concentration,
• frequency of urination, • sleep patterns,
• • mood, as well as
fat and fluid distribution,
secondary sexual characteristics • vision changes,
such as loss or growth of hair, • joint pain, sexual dysfunction.
Health History
• the severity of these changes,
• the length of time the patient has experienced these changes,
• the way in which these changes have affected the patient’s ability to
carry out activities of daily living,
• the effect of the changes on the patient’s self-perception, and
• family history.
Physical Assessment
• Vital signs
• Head to toe inspection
• Palpation of the skin, hair and thyroid
• Physical, psychological, and behavioral changes should be noted such as:
• Hirsutism • edema,
• Moon face • thinning of the skin
• Buffalo humps • Truncal obesity
• Exophthalmos • Obesity
• vision changes, • Changes in mood and behavior
Diagnostic Evaluation
• Blood tests
• Urine tests
• Additional Diagnostic Studies
• Stimulation test
• Suppression tests
• Imaging studies
• Genetic screening
Hypothalamus
• Sits between the cerebrum and
brainstem
• Houses the pituitary gland and
hypothalamus
• Regulates:
• Temperature
• Fluid volume
• Growth
• Pain and pleasure response
• Hunger and thirst
Hypothalamus Hormones
• Releasing and inhibiting hormones
• Corticotropin-releasing hormone
• Thyrotropin-releasing hormone
• Growth hormone-releasing hormone
• Gonadotropin-releasing hormone
• Somatostatin-=-inhibits GH and TSH
Pituitary (hypophysis) Gland
•  Sits beneath the hypothalamus
• Termed the “master gland”
• Divided into:
• Anterior Pituitary Gland
• Growth hormone
• adrenocorticotropic hormone
• thyroid-stimulating hormone
• Follicle stimulating hormone and luteinizing
hormone
• prolactin
• Posterior Pituitary Gland
• Vasopressin or anti diuretic hormones
• Oxytocin
Disorders in Pituitary glands
• Anterior pituitary glands
• Cushing syndrome
• Acromegaly
• Dwarfism
• Posterior Pituitary Glands
• Diabetes insipidus
• SIADH
Diabetes Insipidus
• A disorder of the posterior lobe of the pituitary gland that is
characterized by a deficiency of ADH (vasopressin).
• Excessive thirst (polydipsia) and large volumes of dilute urine.
• It may occur secondary to head trauma, brain tumor, or surgical
ablation or irradiation of the pituitary gland, infections of the central
nervous system or with tumors
• Another cause of diabetes insipidus is failure of the renal tubules to
respond to ADH
Clinical Manifestations
• Polyuria (>250 mL per hour)
• very dilute urine (specific gravity of 1.001 to 1.005)
• Presence of albumin and glucose in the urine
• polydipsia
Assessment and Diagnostic Findings
• fluid deprivation test
• withholding fluids for 8 to 12 hours or until 3% to 5% of the body weight is
lost
• Plasma and urine osmolality studies are performed at the beginning and end
of the test
• inability to increase the specific gravity and osmolality
Medical Management
• to replace ADH (which is usually a long term therapeutic program),
• to ensure adequate fluid replacement, and
• to identify and correct the underlying intracranial pathology.

• Pharmacologic Therapy
• Desmopressin
• Chlorpropamide
• thiazide diuretics
Nursing Management
• Physical assessment
• patient education
Syndrome of Inappropriate Antidiuretic
Hormone Secretion (SIADH)
• excessive ADH secretion from the pituitary gland

• cannot excrete a dilute urine, retain fluids, and develop a sodium

deficiency known as dilutional hyponatremia

• Nonendocrine in origin
• Possible causes:
• Bronchogenic carcinoma
• Lung disorders
• CNS disorders
• Medical Management
• eliminating the underlying cause
• restricting fluid intake if possible
• Diuretics
• Nursing Management
• I and O monitoring
• Daily weight monitoring
• Check for neurologic status
Thyroid Gland
•  Butterfly shaped
• Sits on either side of the trachea
• Has two lobes connected with an isthmus
• Functions in the presence of iodine
• Stimulates the secretion of three
hormones
• thyroxine (T4), triiodothyronine (T3), and
calcitonin
• Involved with metabolic rate management
and serum calcium levels
Thyroid Hormones
• Thyroid hormone is comprised of T4 and T3,
• Both are amino acids that contain iodine molecules
• Iodine is essential to the thyroid gland for synthesis of its hormones
• Secretion of T3 and T4 is controlled by TSH (thyrotropin)
• main function is to control cellular metabolic activity
• Calcitonin – storing calcium from blood into the bones
Diagnostic evaluation
• Serum Thyroid-Stimulating Hormone
• Serum T3 and T4
• T3 -80 to 200 ng/dL (1.2 to 3.1 nmol/L)
• T4 - 5.4 to 11.5 µg/dL (57 to 148 nmol/L)
• T3 Resin Uptake Test
• Radioactive Iodine Uptake
• Fine-Needle Aspiration Biopsy
• Thyroid Scan, Radioscan, or Scintiscan
• Serum Thyroglobulin
Hypothyroidism
• hypothyroidism is the disease state caused by insufficient production of thyroid hormone by
the thyroid gland.
• INCEDENCE
• 30-60 yrs of age
• Mostly women (5 times more than men)
• Causes
• Autoimmune disease (Hashimoto's thyroiditis, post–Graves' disease)
• Atrophy of thyroid gland with aging
• Therapy for hyperthyroidism
• Radioactive iodine (131I)
• Thyroidectomy
• Medications
• Radiation to head and neck
• Infiltrative diseases of the thyroid
 Clinical Manifestations
1. Fatigue. 10. Menstrual disturbances
2. Constipation. 11. Numbness and tingling of fingers.
3. Apathy 12. Tongue, hands, and feet may enlarge
4. Weight gain. 13. Slurred speech
5. Memory and mental impairment and 14. Hyperlipidemia.
decreased concentration.
6. masklike face. 15. Reflex delay.
7. Menstrual irregularities and loss of 16. Bradycardia.
libido. 17. Hypothermia.
8. Coarseness or loss of hair. 18. Cardiac and respiratory complications .
9. Dry skin and cold intolerance.
• Laboratory Test
• T3 T4 TSH

• Treatment
• LIFELONG THYROID HORMONE REPLACEMENT
• levothyroxine sodium (Synthroid, T4, Eltroxin)
• IMPORTANT: start at low does, to avoid hypertension, heart failure and MI Teach about
S&S of hyperthyroidism with replacement therapy
• Administration of high-dose glucocorticoids
MXYEDEMA
• are serious complication of untreated hypothyroidism
• Decreased metabolism causes the heart muscle to become flabby
• Leads to decreased cardiac output
• Leads to decreased perfusion to brain and other vital organs
• Leads to tissue and organ failure
• LIFE THREATENING EMERGENCY WITH HIGH MORTALITY RATE
• Edema changes client’s appearance
• Nonpitting edema appears everywhere especially around the eyes, hands, feet,
between shoulder blades
• Tongue thickens, edema forms in larynx, voice husky
Treatment of Myxedema
• Patent airway Replace fluids with IV.
• Give levothyroxine sodium IV
• Give glucose IV
• Give corticosteroids
• Check temp,
• BP hourly
• Monitor changes LOC hourly
• Aspiration precautions,
• keep warm
Hyperthyroidism
• Hyperthyroidism is the second most prevalent endocrine disorder,
after diabetes mellitus.
• Graves' disease: the most common type of hyperthyroidism, results
from an excessive output of thyroid hormones.
• May appear after an emotional shock, stress, or an infection
• Other causes: thyroiditis and excessive ingestion of thyroid hormone
• Affects women 8X more frequently than men (appears between
second and fourth decade)
• Clinical Manifestations (thyrotoxicosis):
• 1.Heat intolerance.
• 2. Palpitations, tachycardia, elevated systolic BP.
• 3. Increased appetite but with weight loss.
• 4. Menstrual irregularities and decreased libido.
• 5. Increased serum T4, T3.
• 6. Exophthalmos (bulging eyes)
• 7. Perspiration, skin moist and flushed ; however, elders’ skin may be dry and pruritic
• 8. Insomnia.
• 9. Fatigue and muscle weakness
• 10. Nervousness, irritability, can’t sit quietly.
• 11. Diarrhea.
Medical Management
• Radioactive 131I therapy
• Medications
• Propylthiouracil and methimazole
• Sodium or potassium iodine solutions
• Dexamethasone
• Beta-blockers
• Surgery; subtotal thyroidectomy
• Relapse of disorder is common
• Disease or treatment may result in hypothyroidism
Thyroid Storm (Thyrotoxic Crisis)
• form of severe hyperthyroidism, usually of abrupt onset.
• it is almost always fatal, but with proper treatment the mortality rate
is reduced substantially
• requires astute observation and aggressive and supportive nursing
• usually precipitated by stress, such as injury, infection, thyroid and
nonthyroid surgery, tooth extraction, insulin reaction, diabetic
ketoacidosis, pregnancy, digitalis intoxication, abrupt withdrawal of
antithyroid medications, extreme emotional stress, or vigorous
palpation of the thyroid
Clinical Manifestations
• Thyroid storm is characterized by:
• High fever (hyperpyrexia), >38.5°C (>101.3°F)
• Extreme tachycardia (>130 bpm)
• Exaggerated symptoms of hyperthyroidism with disturbances of a major
system—for example, gastrointestinal (weight loss, diarrhea, abdominal pain)
or cardiovascular (edema, chest pain, dyspnea, palpitations)
• Altered neurologic or mental state, which frequently appears as
management
• A hypothermia mattress or blanket
• ice packs
• a cool environment
• hydrocortisone, and acetaminophen (Tylenol)
• Oxygen therapy
• Dextrose IV
• Propylthiouracil (PTU) or methimazole
• Hydrocortisone
• Iodine
Thyroiditis
• Inflammation of the thyroid gland.
• Can be acute, subacute, or chronic (Hashimoto's Disease)
• Each type of thyroiditis is characterized by inflammation, fibrosis, or
lymphocytic infiltration of the thyroid gland.
• Characterized by autoimmune damage to the thyroid.
• May cause thyrotoxicosis, hypothyroidism, or both
Parathyroid Glands
• Embedded within the posterior lobes
of the thyroid gland
• Secretion of one hormone
• Maintenance of serum calcium levels
• (Parathormone) Parathyroid hormone—
regulates serum calcium
Hyperparathyroidism
• caused by overproduction of parathormone
• characterized by:
• bone decalcification
• development of renal calculi (kidney stones) containing calcium.
• 2 to 4X more frequent in women
• 60 and 70 years of age
• Diagnostic Tests:
• Serum calcium
• double-antibody parathyroid hormone tes
Manifestations
• elevated serum calcium, • nausea,
• bone decalcification, • vomiting,
• renal calculi, • constipation,
• apathy, • hypertension,
• fatigue, • cardiac dysrhythmias,
• muscle weakness, • psychological manifestations
Treatment

• Parathyroidectomy
• Hydration therapy
• Encourage mobility reduce calcium excretion
• Diet: encourage fluid, avoid excess or restricted calcium
Hypoparathyroidism
• Deficiency of parathormone usually due to surgery
• Results in hypocalcaemia and hyperphosphatemia
• Manifestations include
• tetany, • anxiety,
• numbness and tingling in extremities, • Irritability,
• stiffness of hands and feet, • depression,
• bronchospasm, • delirium,
• laryngeal spasm, • ECG changes
• carpopedal spasm, • Trousseau’s sign and Chvostek’s sign
Management
• Increase serum calcium level to 9—10 mg/dL
• Calcium gluconate IV
• May also use sedatives such as pentobarbital to decrease neuromuscular
irritability
• Parathormone may be administered; potential allergic reactions
• Environment free of noise, drafts, bright lights, sudden movement
• Diet high in calcium and low in phosphorus
• Vitamin D
• Aluminum hydroxide is administered after meals to bind with phosphate and
promote its excretion through the gastrointestinal tract.
Adrenal glands
• Pyramid-shaped organs that sit on top of the kidneys
• Each has two parts:
• Adrenal Cortex (outer)
• Mineralocorticoid—aldosterone
• Affects sodium absorption, loss of potassium by kidney
• Glucocorticoids—cortisol
• Affects metabolism, regulates blood sugar levels, affects growth,
anti-inflammatory action, decreases effects of stress
• Adrenal androgens—testosterone
• Adrenal Medulla (inner)
• Epinephrine
• Norepinephrine 
Disorders in the Adrenal Glands
• Adrenal Medulla
• Pheochromocytoma
• Adrenal Cortex
• Addison’s Disease
• Cushing’s syndrome
Pheochromocytoma
• Uncommon tumor in the adrenal medulla w/c is usually benign
• High Blood Pressure is the most common cause
• Peak: 40 and 50 years old
Assessment and Diagnostic Findings
• Five “Hs”
• Headache
• Hyperhidrosis
• Hypertension
• Hypermetabolism
• Hyperglycemia
• Diagnostic findings:
• Presence of vanillylmandelic acid and metanephrine in the 24hr urine sample
Management
• Bed rest with head elevated during attacks
• Blood pressure monitoring
Pharmacologic
• alpha-adrenergic blocker (phenoxybenzamine) 10-14 days preop
• Calcium channel blocker
• Surgical
• adrenalectomy
Addison Disease
• primary adrenal insufficiency (PAI)
• occurs when the adrenal glands are damaged and cannot produce
sufficient amounts of cortical hormones
• Autoimmune or idiopathic
• Causes:
• Therapeutic use of corticosteroids – most common
• Infections (Tuberculosis and histoplasmosis – most common)
• Medications (anticoagulants, anticonvulsants, rifampicin)
Clinical Manifestations
• muscle weakness;
• anorexia;
• GI symptoms;
• fatigue;
• emaciation;
• dark pigmentation of the mucous membranes and the skin, especially of the knuckles,
knees, and elbows;
• hypotension;
• low blood glucose,
• low serum sodium, and high serum potassium levels.
• Depression
Addisonian Crisis
• Develops as the disease progress
• Manifestations:
• hypotension, cyanosis, fever, nausea, vomiting, and signs of shock

• Even slight overexertion, exposure to cold, acute infection, or a

decrease in salt intake may lead to circulatory collapse, shock, and
death, if untreated
Assessment and Diagnostic Findings
• Laboratory lab results:
• hypoglycemia
• hyponatremia
• hyperkalemia
• Leukocytosis
• Combined measurement of early morning serum cortisol and plasma
ACTH
Medical Management
• Immediate treatment of shock:
• restoring blood circulation,
• administering fluids and corticosteroids,
• monitoring vital signs, and
• placing the patient in a recumbent position with the legs elevated.
• Hydrocortisone (Solu-Cortef) is administered by IV,
• Vasopressors may be required if hypotension persists
• Antibiotics may be given if infection
Cushing Syndrome
• Due to excessive adrenocortical activity or corticosteroid medications
• Women between the ages of 20 and 40 years are five times more
likely than men to develop Cushing's syndrome.
Clinical Manifestations
• Hyperglycemia • hypertension
• weight gain, • “moon-face”,
• central type obesity with “buffalo hump,” • acne,
• heavy trunk and thin extremities, • increased susceptibility to infection,
• slow healing,
• fragile thin skin,
• virilization in women,
• ecchymosis,
• loss of libido,
• striae,
• mood changes,
• weakness, • increased serum sodium,
• metabolic alkalosis • decreased serum potassium
• lassitude, sleep disturbances, • ↑ Na+ ↑ glucose, ↓ K+,
• osteoporosis, muscle wasting, • metabolic alkalosis

• Diagnosis: Dexamethasone suppression test,

Medical management
• If caused by pituitary tumors – transsphenoidal hypophysectomy
• If caused by adrenal tumors – adrenalectomy
• radiation of the adrenal gland
• Adrenal enzyme inhibitors
• Mitotane
• Ketoconazole
• Tapering of cortecosteroids