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Endocrine Study Guide

The document summarizes several endocrine disorders including: 1. Diabetes insipidus results from a deficiency of ADH leading to diluted urine and concentrated serum, while SIADH is caused by excessive ADH causing concentrated urine and diluted serum. 2. Hyperthyroidism is due to excessive thyroid hormones, decreasing TSH and increasing T3, while hypothyroidism increases TSH and decreases T3, T4, and free thyroxine. 3. Cushing's disease results from excess glucocorticoids, increasing cortisol, sodium, and glucose, while Addison's disease decreases these factors due to adrenocortical insufficiency.
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100% found this document useful (1 vote)
1K views4 pages

Endocrine Study Guide

The document summarizes several endocrine disorders including: 1. Diabetes insipidus results from a deficiency of ADH leading to diluted urine and concentrated serum, while SIADH is caused by excessive ADH causing concentrated urine and diluted serum. 2. Hyperthyroidism is due to excessive thyroid hormones, decreasing TSH and increasing T3, while hypothyroidism increases TSH and decreases T3, T4, and free thyroxine. 3. Cushing's disease results from excess glucocorticoids, increasing cortisol, sodium, and glucose, while Addison's disease decreases these factors due to adrenocortical insufficiency.
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© Attribution Non-Commercial (BY-NC)
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Posterior pituitary disorders: (this gland secretes ADH and Vasopressin)

Diabetes Insipidus 1. Overview: results from deficiency of ADH, which results in excessive diluted urination, excessive thirst, excessive fluid intake 2. Subjective data: a. polyuria (5 to 20L/ day) b. polydipsia c. Nocturia d. Fatigue e. Dehydration 3. Objective Data: a. Urine chemistry is Diluted!: decreased urine specific gravity, decreased urine osmolality, decreased urine pH, decreased urine sodium/potasium, (as urine volume increases, urine osmlality decreases) b. Serum chemistry is Concentrated!: increased serum osmolality, increase serum sodium/potassium, (as serum volume decreases, serum osmolality increases) c. radioimmunoassay: decreased ADH 4. Diagnostic procedures: water deprivation test, vasopressin test 5. Nursing care: monitor urine output, central venous pressure, I and O, labs, weigh client daily, add bulk foods if constipation develops 6. Medications: ADH replacement agents (Desmopressin), ADH stimulants (Carbamazepine/Tegretol), Vasopressin 7. Complications: hypovolemia, hyperosmolarity, hypernatremia, circulatory collapse, unconsciousness Syndrome of inappropriate antidiuretic hormone (SIADH) 1. Overview: excessive release of ADH (Vasopressin), leads to excessive water reabsorption, supression of renin-angiotensin mechanism, water intoxication, cellular edema, dilutional hyponatremia, fluid shifts 2. Subjective data: a. H/A, weakness, anorexia, muscle cramps, weight gain (without edema b/c water NOT sodium is retained) b. as serum sodium decreases client experiences personality changes, hostility, sluggish tendon reflexes, nausea, vomiting 3. Objective data: a. Urine chemistry is Concentrated!: increased urine sodium, increase urine osmlarity (as urine voume decreases, urine osmolarity increases) b. Serum chemistry is Diluted!: decreased serum sodium, decreased serum osmolarity, (as serum volume increases, serum osmolarity decreases) c. Radioimmunoassay; increased ADH 4. Diagnostic procedures: ATI states none 5. Nursing care: restrict oral fluids (500 to 1000ml/day) to prevent hemodilution (first priority), I and Os, monitor for signs of increased BP, tachycardia, hypothermia, 6. Medications: Demeclocycline (may cause drug-induced diabetes insipidus), Lithium (blocks renal response to ADH, Lasix (increase water excretion from kidneys) 7. Complications: water intoxication, Central pontine myelinolysis(nerve damage that is caused by destructino of myeline sheath)

Thyroid disorders: (produces T4, T3, and thyrocalcitonin)


Hyperthyroidism: 1. Overview: excessive of circulating thyroid hormones, results in exaggerating body functions/ hypermetabolic state, Graves disease is most common cause 2. Subjective data: nervousness, hyperactivity, emotional lability, weakness, heat intolerance, weight loss, insomnia, frequent stool/diarrhea, warm flushed skin, tremor, vision changes

3. Objective data: a. physical assessment: bruit over thyroid gland, high systolic pressure b. tachycardia b. TSH is Decreased! (due to negative feedback loop) c. T3 elevated 4. Diagnostic procedures: radioiodine uptake and thyroid scan 5. Nursing care: minimize energy expenditure, promote calm, nutritional status, provide eye protection for patients with exophthalmos (eye disorder), EKG for dysrhythmias 6. Medications: a. Propylthiouracil (PTU) or methimazol (Tapazole), act by blocking thyroid homrone synthesis (divide doses at regular intervals), b. Propranolol (treats sympathetic nervous system effects such as tachycardia), c. Saturated solution of potassium iodide (SSKI): inhibits release of stored thyroid hormone (short term use only) 7. Procedures/interventions: a. radioactive iodine therapy: destroys hormone producing cells b. thyroidectomy 8. Complications: a. thyroid storm (sudden surge of large amount of thyroid hormones into bloodstream, medical emergency with high mortality rate) b. Hypocalcemia/tetany c. nerve damage Hypothyroidism: 1. Overview: inadequate amount of circulating thyroid hormones, results in decreased metabolic rates a. Primary: dysfunction of thyroid gland b. Secondary: failure of anterior pituitary gland to stimulate thyroid gland c. Tertiary: failure of hypothalamus to produce thyroid releasing factor 2. Subjective data: a. early findings: fatigue, intolerance to cold, decreased bowel motility, weight gain, thing brittle fingernails, depression, thinning hair b. late findings: slow thought process, thickening of skin, thinning of hair, swelling of face, hands, hoarse speech, abnormal menstrual periods, 3. Objective data: a. Decreased T3 b. Elevated TSH (due to negative feedback loop) c. Decreased free thyroxin and T4 levels d. Elevated serum cholesterol e. Anemia 4. Diagnostic Procedures: Skull xray, CT, MRI, radioisotope scan and uptake, EKG 5. Nursing care: monitor for CV changes (low BP, bradycardia), apply antiembolism stockings and elevate legs to assist venous return, low calorie/bulk diet to encourage activity to prevent constipation 6. Medications: Thyroid hormone replacement: levothyroxine (Synthroid): drug of choice 7. Complications: Myxedema coma (life threatening, a stressor such as infection has severe effects during hypothyroid state

Adrenal Disorders: produces Aldosterone, Glucocorticoids, Sex hormones) note:


Aldosterone increases sodium absorption, cases potassium excretion Glucocorticoids (cortisol): affects glucose, protein, fat metabolism, response to stress

Cushing Disease

1. Overview: excess of glucocorticoids, results in increased cortisol and increased androgens 2. Subjective data: weakness, fatigue, back and joint pain, altered emotional state 3. Objective data a. decreased immune function, decreased inflammatory response, thin fragile skin, bruising, hypertension, tachycardia, weight gain, dependent edema (moon face, truncal obesity, buffalo hump), impaired glucose tolerance, red cheeks, striae b. elevated plasma cortisol levels in the absence of acute illness c. elevated ACTH (adrenocorticotropic hormone) d. decreased potassium and calcium levels e. increased serum sodium and glucose levels f. decreased lymphocytes 4. Diagnostic Procedures: xray, MRI, CT to identify lesions of pituitary gland, adrenal gland, lung, GI tract or pancreas. Radiologic imaging 5. Nursing care: decrease sodium intake, increase potassium/protein/calcium intake, sign for hypervolemia, prevent infection 6. Medications: a. aminoglutethimide (Cytadren): adrenal corticosteroid inhibitor, use no more than 3 months (usually for surgery) b. Ketoconacole (Nizoral): Adrenal corticosteroid inhibitor 7. Therapeutic procedures: a. chemo (if caused by tumor) b. hypophysectomy, removal of pituitary gland 8. Complications: viscera/ulceration in lining of stomach, risk for bone fractures, immunosuppression, Addisons Disease 1. Overview: adrenocortical insufficiency, caused by damage or dysfunction of adrenal cortex, mineralocorticoids and glucocorticoids is diminished 2. Subjective: signs develop slowly, hyperpigmentation, weakness, fatigue, nausea, dizziness, dehydration, hyponatremia, hyperkalemia, hypoglycemia, hypercalcemia 3. Objective: a. increase potassium, calcium b. decreased sodium c. decreased serum glucose/ cortisol 4. Diagnostic procedures: EKG, Xray, CT and MRI to determine source of adrenal insufficiency 5. Nursing care: monitor for fluid deficits, hyponatremia, restore fluid volume, monitor for hypoglycemia, 6. Medications: a. hydrocortisone, prednisone, cortisone: glucocorticoids used as adrenocorticoid replacement b. fludrocortisone: mineralcorticoid used as replacement 7. Complications: a. Addisonian crisis: occurs with acute drop in adrenocorticoids due to sudden discontinuatino of glucocorticoid meds or when induced by severe trauma or stress b. hypoglycemia c. hyperkalemia/hyponatremia

Diabestes insipidus

Deficiency of ADH

Urine diluted

Serum concentrated

SIADH

Excessive ADH

Urine concentrated

Serum diluted

Hyperthyroidism Hypothyroidism

excessive throid homrones decrease thyroid hormones

Decreased TSH Increased TSH

Increased T3 Decreased T3, T4, free thyroxin

Cushings

excess of glucocorticoids, adrenocortical insufficiency

increased cortisol, sodium and glucose decrease cortisol, sodium and glucose

decrease potassium and calcium, and lymphocytes increase potassium, calcium

Addisons

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