Professional Documents
Culture Documents
UNIT I
Assessment and
Management of Patients
With Endocrine Disorders
Endocrine System
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
Hormones
Steroid: act inside the cell
Peptide (protein): act on cell surface
Amine
Fatty acid derivative
Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins
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Hypothalamus
Hormones
CRH
TRH
GHRH
GnRH
Somatostatin
Control the release pituitary hormones
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Hormone Secretion
Definition
Etiology
Assessment
Management
Eliminate cause
Fluid restriction
Diuretics (furosemide,Lasix)
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HPT axis
Hypothalamic-Pituitary-Thyroid Axis
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Thyroid Hormones
Thyroid
Thyroid hormones: T3, T4 also produces calcitonin
Iodine is contained in thyroid hormone
TSH from the anterior pituitary controls the release of
thyroid hormone
TRH from the hypothalamus controls the release of TSH
Thyroid hormone controls cellular metabolic activity
T3 is more potent and more rapid-acting than T4
Calcitonin is secreted in response to high plasma calcium
level and increases calcium deposition in bone
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Thyroid Disorders
Hypothyroidism- myxedema,
Hashimotos disease
Hyperthyroidism- Graves Disease
Thyroiditis
Thyroid Tumors
Endemic (Iodine-Deficient) Goiter
Nodular Goiter- hyperplasia
Thyroid Cancer
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Hypothyroidism
Cretinism: Inadequate secretion of thyroid
Hypothyroidism
Hypothyroidism
Causes: Autoimmune thyroiditis; Hashimotos disease (most
common cause)
(See Chart 42-2)
Affects women 5X more frequently than men
Manifestations:
Early symptoms may be nonspecific
Fatigue; hair, skin and nail changes; numbness and
tingling of fingers; menstrual disturbances, subnormal
temperature and pulse; weight gain; subdued
emotional and mental responses; slow speech; tongue,
hands, and feet may enlarge; personality and cognitive
changes; cardiac and respiratory complications
Myxedema may progress to stupor, coma, and death
Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins
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Hypothyroidism: Medical
Management
Medical Management of Hypothyroidism
Synthetic levothyroxine-replacement therapy
Medication interactions
Effects of hypnotic and sedative agents; reduce dosage
Support of cardiac function and respiratory function
Prevention of complications
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Hyperthyroidism
Hyperthyroidism
The second most prevalent endocrine disorder
Excessive output of thyroid hormone
Graves disease (most common cause)
Affects women 8X more frequently than men
Manifestationsthyrotoxicosisnervousness;
palpitations; rapid pulse; tolerate heat poorly; tremors;
skin is flushed, warm, soft, and moist; however, elders
skin may be dry and pruritic; exophthalmos, increased
appetite and dietary intake; weight loss; elevated systolic
BP; may progress to cardiac dysrhythmias and failure
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Thyroid Storm
Manifestations:
High fever, extreme tachycardia, exaggerated
symptoms of hyperthyroidism, delirium, coma,
somnolence.
Treatment
Hypothermia blanket, ice packs, cool
environment, Tylenol, humidified O2, ABGs, IVF
with dextrose, PTU, hydrocortisone to treat shock
or adrenal insufficiency, Iodine, Beta Blocker,
propranolol + digoxin for cardiac rhythm
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Medical Management of
Hyperthyroidism
Radioactive 131I therapy
Medications
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Medical Management of
Hyperthyroidism
Radioactive 131I therapy
Medications
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Thyroidectomy
Treatment of choice for thyroid cancer
Cancer surgery may include modified or radical neck
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Postoperative Care
Monitor dressing for potential bleeding and
Nursing Management of
Hyperthyroidism : Medical
Assessment
Nursing Diagnoses
Imbalanced nutrition: Less than body requirements
Ineffective coping r/t irritability
Low self-esteem r/t changes in appearance
Altered body temperature
Nursing Interventions
Teaching
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Question
Which medication blocks synthesis of thyroid
hormone?
A. Dexamethasone
B. Methimazole
C. Potassium iodide
D. Sodium iodide
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Answer
B
Methimazole blocks synthesis of thyroid
hormone. Dexamethasone, potassium
iodide, and sodium iodide suppress release
of thyroid hormone.
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Parathyroid
Four glands on the posterior thyroid gland
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.
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Parathyroid Disorders
Hyperparathyroidism-
characterized by bone
decalcification and development of
renal calculi
Hypoparathyroidism- occurs
frequently with thyroidectomy or
radical neck dissection
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Hyperparathyroidism
Primary hyperparathyroidism is 24X more frequent in
women.
Manifestations include elevated serum calcium, bone
decalcification, renal calculi, apathy, fatigue, muscle
weakness, nausea, vomiting, constipation, hypertension,
cardiac dysrhythmias, psychological manifestations
Treatment
Parathyroidectomy
Hydration therapy
Encourage mobility reduce calcium excretion
Diet: encourage fluid, avoid excess or restricted calcium
Hypercalcemic crisis
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Hypoparathryoidism
Deficiency of parathormone usually due to surgery
Management of
Hypoparathyroidism
Question
Is the following statement True
or False?
The patient in acute
hypercalcemic crisis requires
close monitoring for lifethreatening complications and
prompt treatment to reduce
serum calcium levels.
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Answer
True
The patient in acute hypercalcemic crisis
requires close monitoring for lifethreatening complications and prompt
treatment to reduce serum calcium levels.
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Adrenal Cortex
Glucocorticoids
Mineralocorticoids
Androgens
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Adrenal Disorders
Pheochromocytoma- benign tumor
Adrenocortical Insufficiency (Addisons
Pheochromocytoma
Benign (usually) tumor of adrenal medulla
Peak 40-50 years of age
Familial tendency
Clinical manifestations
Headache, palpitations, diaphoresis
Hypertension common; hyperglycemia
Acute, unpredictable attacks of extreme
anxiety, tremulous, weak, air hunger and others
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Pheochromocytoma
Assessment/Diagnostic tests
5 Hs: hypertension, hyperhydrosis,
hypermetabolism, hyperglycemia, headache
Urine & plasma levels of catecholamines
Urine:Metanephrines, Vanillylmandelic acid (VMA)
24 hour urine; restrict coffee, tea, vanilla, chocolate,
bananas, & ASA as may alter test results
Plasma catecholamine measured with patient supine
and at rest for 30 minutes; venous access placed
before start the test
Other tests, p. 1277
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Pheochromocytoma
Management: Bedrest with HOB elevated to
reduce BP
Pharmacologic therapy
Alpha adrenergic blockers: phentolamine (Regitine) or
smooth muscle relaxants: sodium nitroprusside
(Nipride) to lower BP
Long acting alpha blocker: phenoxybenzamine
(Dibenzyline) to reduce BP in preparation for surgery.
Beta adrenergic blockers for cardiac dysrhythmias/
tachycardia and angina (propranolol [Inderal])
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Pheochromocytoma
Surgical management: definitive treatment is
Pheochromocytoma
Nursing Mangement
Monitoring VS, F/E balance, blood glucose
Administer corticosteroids as ordered
Teaching
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Adrenocortical Insufficiency
Addisons disease: may result from autoimmune or idiopathic
atrophy
May be the result of adrenal suppression by exogenous
steroid use
Manifestations include muscle weakness, anorexia, GI
symptoms, fatigue, dark pigmentation of skin and mucosa,
hypotension, low blood glucose, low serum sodium, high
serum potassium, mental changes, apathy, emotional lability,
confusion
Addisonian crisis: Circulatory shock, may be precipitated by
low salt intake, surgery, exposure to cold, infection.
Diagnostic tests; adrenocortical hormone levels, ACTH
levels, ACTH stimulation test
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Addisons Disease
Diagnostic tests
Low blood glucose
Hyponatremia
Hyperkalemia
Leukocytosis
Low serum cortisol
ACTH administration No response of plasma
cortisol increase (if adrenal cortex is destroyed)
and urinary 17-hydroxycorticosteroids
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Addisons Disease
Medical Management
Reduce shock: fluids, IV corticosteroids
(Hydrocortisone/Solu-Cortef), recumbent
position with legs elevated.
Treat cause, e.g. infection
Lifelong corticosteroids (prednisone) &
mineralocorticoids (Florinef) may be necessary;
added glucocorticoids with stressor; added salt
during times of fluid loss
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Addisons Disease
Nursing Management
Assessment
Managing Addisonian crisis
Restoring fluid balance (Florinef & prednisone)
Improving activity tolerance
Teaching: Home care checklist, p. 1280
Need written and verbal discharge instructions
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Cushings Syndrome
Definition: Excessive adrenocortical
activity
Etiology
Excessive corticosteroid administration*
Excessive ACTH
Hyperplasia of adrenal cortex
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Cushings Syndrome
Clinical manifestations
Central-type obesity
Buffalo hump: fatty tissue in neck and supraclavicular
areas
Thin extremities
Skin: fragile, ecchymoses, striae,
Weakness
Osteoporosis, compression fractures
Retention of sodium & water (mineralocorticoid)
Moon face, acne, oily skin
Hyperglycemia;increased susceptibility to infection
Weight gain
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Cushings Syndrome
Diagnostic findings
Increased serum sodium & blood sugar
Decreased K+
Decreased eosinophils, and lymphoid tissue
Dexamethasone suppression test, overnight
Give 1mg of oral dexamethasone at 11PMblood
draw at 8AM. If cortisol suppressed to <5mg/dL,
then the HPA axis is working properly
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Cushings Syndrome
Medical Management
Pituitary tumor as cause
Surgical removal of tumor by transsphenoidal
hypophysectomy: Incision made beneath upper lip to reach
pituitary gland through sphenoid sinus (Chapter 61)
Monitor fluid status: DI can occur
No coughing, blowing nose, or sneezing as may lead to CSF
leak
Assess nasal drainage for glucose, if + CSF
Halo sign on dressing: light yellow at edge of clear drainage:
CSF
Cushings Syndrome
Nursing management
Assessment
Nursing Diagnoses
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Interventions
Decrease risk of injury; establish a protective environment;
Corticosteroid Therapy
Uses- adrenal insufficiency, inflammation,