Fluid and Electrolyte Imbalance - Endocrine Flashcards
Check for method of handling hormone test samples
note tube type, timing, drugs to be administered as part of the test, etc
Patient education about test
explain procedure and any restrictions to the patient
If you are drawing blood sample from a line
clear the IV line thoroughly; do not use a double- or triple-lumen line to obtain samples
If drug is prescribed for the test
Emphasize the importance of taking drug on time; tell pt to set alarm if the drug is to be taken at night
Urine collection
instruct pt to begin the urine collection by first emptying his or her bladder; do not save this urine; note time and plan to collect all urine from this time until the end of the collection period
To end urine collection
empty his or her bladder at the end of the timed period and add that to the collection
Storage and handling
is preservative needed (add to beginning), does sample need to be kept cold (place the container in cooler with ice)
Hormone replacement for acute adrenal insufficiency
Start rapid infusion of NS or D5NS; hydrocortisone sodium succinate 100-300 mg or dexamethasone 4-12 mg as IV bolus; 100 mg hydrocortisone sodium succinate via IV over next 8 hrs; hydrocortisone 50 mg IM every 12 hrs; H2 histamine blocker IV for ulcer prevention
Hyperkalemia management for acute adrenal insufficiency
administer insulin with dextrose in NS to shift K+ into cells; admin K+ binding and excreting resin; give loop or thiazide diuretics; avoid K+-sparing diuretics; initiate K+ restriction; monitor input/output; monitor HR, rhythm, and ECG for manifestations of hyperkalemia
Hypoglycemia management for acute adrenal insufficiency
administer IV glucose; administer glucagon; maintain IV access; monitor blood glucose hourly
Causes of primary adrenal insufficiency
autoimmune disease, TB, metastatic cancer, fungal lesions, AIDS, hemorrhage, gram-negative sepsis, adrenalectomy, abdominal radiation therapy, drugs and toxins
Causes of secondary adrenal insufficiency
pituitary tumors, postpartum pituitary necrosis, hypophysectomy, high-dose pituitary radiation, high-dose whole-brain radiation
Adrenal gland hypofunction history
changes in activity level, salt intake, anorexia, N/V, diarrhea, abdominal pain, weight loss, radiation to abdomen or head, and past and current drugs
Neuromuscular manifestations of adrenal insufficiency
muscle weakness, fatigue, joint/muscle pain
GI manifestations of adrenal insufficiency
anorexia, N/V, abdominal pain, bowel changes, weight loss, salt craving
Skin manifestations of adrenal insufficiency
vitiligo, hyperpigmentation
Cardiovascular manifestations of adrenal insufficiency
anemia, hypotension, hyponatremia, hyperkalemia, hypercalcemia
Psychosocial manifestations of adrenal insufficiency
lethargy, depression, confusion, psychotic, fearful
Increased lab values in adrenal insufficiency
potassium, calcium, bicarbonate, BUN, eosinophil, ATCH
Decreased lab values in adrenal insufficiency
sodium, glucose, cortisol, urinary 17-hydroxycorticosteroids, 17-ketosteroids
Nursing interventions for adrenal insufficiency
daily weight, intake/output, VS every 1-4 hrs, monitor lab values
Correction of cortisol and aldosterone deficiencies
hydrocortisone corrects glucocorticoid deficiency; mineralcorticoid hormone may be needed to maintain electrolyte balance
Hypersecretion by the adrenal cortex results in
hypercortisolism, Hyperaldosteronism, or excessive androgen production
Hypercortisolism (Cushing’s Disease)
exaggerated secretion of cortisol from the adrenal cortex; caused by problem in adrenal cortex, anterior pituitary gland, or hypothalamus; glucocorticoid therapy can also lead to hypercortisolism
Causes of endogenous secretion (Cushing’s Disease)
bilateral adrenal hyperplasia, pituitary adenoma increasing the production of ACTH, malignancies (carcinomas of the lung, GI tract, pancreas), and adrenal adenomas or carcinomas
Hypercortisolism patient history
health problems, drug therapies, age, gender, usual weight, changes in activity, sleep patterns, fatigue, and muscle weakness, bone pain, fractures, frequent infections, easy bruising, menses, and ulcer formation
General appearance of hypercortisolism
fat redistribution (moon face, buffalo hump, truncal obesity), weight gain
Cardiovascular manifestations of hypercortisolism
hypertension, increased risk for thromboembolic events, frequent dependent edema, capillary fragility (bruising, petechiae)
Musculoskeletal manifestations of hypercortisolism
muscle atrophy, osteoporosis (pathologic fractures, decreased height with vertebral collapse, aseptic necrosis of the femur head, slow or poor healing of bone fractures)
Skin manifestations of hypercortisolism
thinning skin, striae, increased pigmentation
Immune system manifestations of hypercortisolism
increased risk for infection, decreased immune function, decreased inflammatory responses, decreased production of pro-inflammatory cytokines, histamine, and prostaglandins, manifestations of infection/inflammation may be masked
Psychosocial manifestations of hypercortisolism
emotional instability, mood swings, irritability confusion, depression, inappropriate laughter or crying, difficulty concentrating, neurotic or psychotic behavior, sleep difficulties, and fatigue
Increased lab values in hyperfunction of adrenal gland
sodium, glucose, cortisol, ACTH (pituitary Cushing’s)
Decreased lab values in hyperfunction of adrenal gland
potassium, calcium, bicarbonate, ACTH (adrenal Cushing’s)
Causes of exogenous administration (Cushing’s Syndrome)
therapeutic use of ACTH or glucocorticoids (most commonly used for asthma, autoimmune disorders, organ transplantation, cancer chemo, allergic responses, chronic fibrosis
Patient safety for hypercortisolism
prevent fluid overload from becoming worse; monitor for increased fluid overload (bounding pulse, increasing neck vein distention, lung crackles, increasing peripheral edema, reduced urine output); use pressure-reducing or pressure-relieving overlay on mattress; assess skin pressure areas; change positions every 2 hrs
Drug therapy for hypercortisolism
aminoglutethimide, metyrapone, cyproheptadine, mitotane
Nutrition therapy for hypercortisolism
restrictions of fluid and sodium
Radiation therapy for hypercortisolism
not always effective; often destroys normal tissue; monitor for changes in the pts neurologic status
Surgical therapy for hypercortisolism
removal of pituitary adenoma, hypophysectomy, or adrenalectomy
Preop care
balance and monitor electrolytes; control hyperglycemia; at risk for infections and fractures, monitor for safety; high-calorie, high protein diet; glucocorticoid preparation
Postop care
assess for shock; monitor VS, hemodynamic variables, intake/output, daily weight, serum electrolytes; glucocorticoid and mineralcorticoid replacement
Preventing skin injury for hypercortisolism
instruct pt to avoid activities that can result in skin trauma, use a soft toothbrush and electric shaver; keep skin clean and dry, use moisturizing lotion; us tape sparingly; exert pressure over puncture site longer than normal to prevent bleeding and bruising
Preventing pathologic fractures in hypercortisolism
teach pt safety issues and dietary needs; use lift sheet; call for help when ambulating; use fall precautions; eat high-calorie diet, increased calcium and vit D; avoid caffeine and alcohol
Preventing GI bleeding in hypercortisolism
take antacids on regular schedule; reduce or eliminate habits that contribute to gastric irritation; avoid NSAIDs, ASA, and other salicylates
Protection from infection in hypercortisolism
handwashing; upper respiratory infection caregivers or visitors should wear mask; strict procedures for dressing changes and invasive procedures; continuously assess for possible infection; monitor daily CBC with diff, WBC and absolute neutrophil count; inspect mouth for lesions and mucosa breakdown; assess lungs; ask about urgency, burning, or pain with urination; take VS every 4 hrs; use good personal hygiene and pulmonary hygiene, cough and deep breathe or sustained maximum inhalations hourly
Self-management for hypercortisolism
monitor weight at home, notify provider if pt gains more than 3 lbs in a week or more than 1-2 lbs in 24 hrs; lifelong hormone replacement is needed after bilateral adrenalectomy; protect pt from infection, use proper hygiene, avoid crowds or others with infection, yearly influenza for pt and family, notify provider of fever or other signs of infection; wear medical alert bracelet
Hypophysectomy
surgical removal of the pituitary gland and tumor; most common treatment for hyperpituitarism
Preop care for hypophysectomy
explain that procedure decreases hormone levels, relieves headaches, and may reverse changes in sexual functioning; these changes are usually not reversible; nasal packing will be present for 2-3 days after surgery, breathe through mouth, mustache dressing under nose; instruct not to brush teeth, cough, sneeze, blow nose, or bend forward after surgery due to increased ICP and healing delay
Postop care for hypophysectomy - neuro
monitor neuro status, changes in vision or mental status, altered LOC, decreased strength of extremities, diabetes insipidus, CSF leakage, infection, ICP
Postop care for hypophysectomy - general
monitor fluid balance, maintain pulmonary hygiene, do not cough, blow nose, or sneeze, use dental floss and oral mouth rinses, avoid bending at the waist, monitor nasal drip pad (presence of halo sign may indicate CSF leak), monitor bowel movements to prevent constipation, teach pt self-administration of prescribed hormones
Hyperthyroidism
excessive thyroid hormone secretion from the thyroid gland; thyroid hormones increase metabolism in all body organs; may be temporary or permanent; over-secretion changes the secretion of hormones from the hypothalamus and anterior pituitary gland through negative feedback
Toxic diffuse goiter (Grave’s Disease)
autoimmune disorder in which antibodies are made and attach to the thyroid stimulating hormone (TSH) receptors on the thyroid tissue; the gland enlarges and forms a goiter and overproduces thyroid hormones; exophthalmos and pretibial myxedema are present
Toxic multinodular goiter
caused by multiple thyroid nodules; may be enlarged thyroid tissues or benign tumors; usually have a goiter for years
Exogenous hyperthyroidism
caused by excessive use of thyroid replacement hormones
Patient history of hyperthyroidism
age, gender, usual weight, heat intolerance, palpitations or chest pain, changes in breathing patterns, visual changes, change in energy levels, irritable or depressed, change in menses, increase in libido, medical history, previous thyroid surgery or radiation therapy to the neck, past and current drugs
Skin manifestations of hyperthyroidism
diaphoresis, fine, soft, silky body hair, smooth, warm, moist skin, thinning of scalp hair
Pulmonary manifestations of hyperthyroidism
SOB with or without exertion, rapid, shallow respirations, decreased vital capacity
Cardiovascular manifestations of hyperthyroidism
palpitations, chest pain, increased systolic blood pressure, widened pulse pressure, tachycardia, dysrhythmias
GI manifestations of hyperthyroidism
weight loss, increased appetite, increased stools, hypoproteinemia
Musculoskeletal manifestations of hyperthyroidism
muscle weakness and wasting
Neurologic manifestations of hyperthyroidism
blurred or double vision, eye fatigue, corneal ulcers or infections, increased tears, injected conjunctiva, photophobia, eyelid retraction or lag, globe lag, hyperactive deep tendon reflexes, tremors, insomnia
Metabolic manifestations of hyperthyroidism
increased basal metabolic rate, heat intolerance, low-grade fever, fatigue
Psychological/emotional manifestations of hyperthyroidism
decreased attention span, restlessness, irritability, emotional lability, manic behavior
Reproductive manifestations of hyperthyroidism
amenorrhea, decreased menstrual flow, increased libido
Other manifestations of hyperthyroidism
goiter, wide-eyed or startled appearance (exophthalmos), decreased total WBC, enlarged spleen
Lab testing for hyperthyroidism
triiodothyronine (T3), thyroxine (T4), T3 resin uptake (T3RU), and thyroid-stimulating hormone (TSH); antibodies to TSH (TSH-RAb) are measured to diagnose Graves’ disease
Lab abnormal values for hyperthyroidism
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Thyroid scan
evaluates the position, size, and functioning of the thyroid gland; pregnancy should be ruled out before scan; procedures that use iodine-containing dye should not be performed for at least 4 weeks before a thyroid scan is done; drugs that contain iodine should be discontinued for 1 week before the scan
Ultrasonography
determines the size and general composition of any masses or nodules; takes about 30 minutes and is painless
Drug therapy: thionamides (pylthiouracil and methimazole
block thyroid hormone production by preventing iodide binding in the thyroid gland; PTU prevents T4 from being converted to T3; response is delayed
Drug therapy: iodine preparations
short-term therapy before surgery; decrease blood flow through the thyroid gland; reduces the production and release of thyroid hormone; monitor for hypothyroidism
Drug therapy: lithium
inhibits thyroid hormone release; use is limited d/t side effects of depression, diabetes insipidus, tremors nausea, vomiting; may be used for pt who cannot tolerate other antithyroid drugs
Drug therapy: Beta-adrenergic blocking drugs (propranolol)
supportive therapy; relieves diaphoresis, anxiety, tachycardia, palpitations; do not inhibit thyroid hormone production
Drug therapy: radioactive iodine (RAI) therapy
not used in pregnant women; dosage depends on thyroid gland size and sensitivity to radiation; symptom relief may not occur until 6-8 weeks after therapy; add’l drug therapy is needed during the first few weeks after RAI tx; performed on outpt basis; 1-3 doses needed; radiation dose is low and eliminated in a month; use radiation precautions; monitor regularly for changes in thyroid function
Total and subtotal thyroidectomy
Removal of all or part of the thyroid tissue; decreases the production of thyroid hormones; pt must take lifelong thyroid hormone replacement
Preop care for thyroidectomy
pt is treated with antithyroid drugs; iodine preps are used to decrease thyroid size and vascularity; cardiac issues must be controlled; pt follows high-protein, high-carb diet for days/weeks; teach to support neck while coughing or moving following; hoarseness may be present following; explain the surgery and care following
Operative care for thyroidectomy
general anesthesia; collar incision just above the clavicle; subtotal remaining thyroid tissue is sutured to trachea
Postop care for thyroidectomy
monitor VS 15 min till pt stable then 30 min for 24 hrs; semi-fowlers when awake; sandbags or pillows to support head/neck; avoid neck extention; pain control; humidified air; monitor for hemorrhage, respiratory distress, hypocalcemia, tetany, and laryngeal nerve damage, thyroid storm/crisis
Thyroid storm/crisis triggers
stressors such as trauma, infection, diabetic ketoacidosis, pregnancy, vigorous palpation of goiter, exposure to iodine, radioactive iodine therapy
Thyroid storm/crisis manifestations
fever, tachycardia, systolic hypertension, abdominal pain, nausea, vomiting, diarrhea, as crisis progresses: anxiousness, tremors, restless, confusion, psychotic, seizures leading to coma, can lead to death; report a temp increase of even 1 degree F, as it may indicate an impeding thyroid crisis
Medications during thyroid storm/crisis
methimazole, propylthiouracil, sodium iodide solution, propranolol, glucocorticoids (hydrocortisone, prednisone, or dexamethasone, non-salicylate antipyretics
Emergency care during thyroid storm/crisis
maintain patent airway, administer meds; monitor for cardiac dysrhythmias, VS Q30m; comfort measures, cooling blanket; correct dehydration with NS; cooling blanket or ice packs to reduce fever
Hypothyroidism - Myxedema
thyroid cells fail to produce sufficient levels of thyroid hormones; low metabolic rate; buildup of glycosaminoglycans forms cellular mucinous edema and changes the pts appearance; nonpitting edema forms everywhere
Skin manifestations of hypothyroidism
cool, pale, yellowish, dry, coarse, scaly skin, thick, brittle nails, dry, coarse, brittle hair, decreased hair growth, loss of eyebrow hair, poor wound healing
Pulmonary manifestations of hypothyroidism
hypoventilation, pleural effusion, dyspnea
Cardiovascular manifestations of hypothyroidism
bradycardia, dysrhythmias, enlarged heart, decreased activity tolerance, hypotension
Metabolic manifestations of hypothyroidism
decreased basal metabolic rate, decreased body temperature, cold intolerance
Musculoskeletal manifestations of hypothyroidism
muscle aches and pains, delayed contraction and relaxation of muscles
Neurologic manifestations of hypothyroidism
slowing of intellectual functions (slow or slurred speech, impaired memory, inattentiveness), lethargy or somnolence, confusion, hearing loss, paresthesia of extremities, decreased tendon reflexes
Psychological/emotional manifestations of hypothyroidism
apathy, depression, paranoia, withdrawal
GI manifestations of hypothyroidism
anorexia, weight gain, constipation, abdominal distention
Reproductive manifestations (women) of hypothyroidism
changes in menses, anovulation, decreased libido
Reproductive manifestations (men) of hypothyroidism
decreased libido, impotence
Other manifestations of hypothyroidism
periorbital edema, facial puffiness, nonpitting edema of the hands and feet, hoarseness, goiter, thick tongue, increased sensitivity to opioids and tranquilizers, fatigue, weakness, decreased urine output, anemia, easy bruising, iron deficiency, folate deficiency, B12 deficiency
Primary causes of hypothyroidism
decreased thyroid tissue (surgical removal of thyroid, radiation induced thyroid destruction, autoimmune thyroid destruction, congenital thyroid agenesis, congenital thyroid hypoplasia, congenital thyroid dysgenesis, cancer), decreased synthesis of thyroid hormone (endemic iodine deficiency, excessive exposure to iodine, drugs [lithium, phenylbutazone, propylthiouracil, sodium or potassium percholate, and aminoglutethimade])
Secondary causes of hypothyroidism
inadequate production of thyroid-stimulating hormone (pituitary tumors, trauma, infections, or infarcts, congenital pituitary defects, hypothalamic tumors, trauma, infections, or infarcts)
Pt history for hypothyroidism
compare activity now with that of a year ago; ask whether more blankets at night or sweaters and extra clothing in warm weather have been needed; current or previous use of drugs; has pt ever been treated for hyperthyroidism, if so what specific treatment was used
Laboratory assessment for hypothyroidism
Triiodothyronine (T3), thyroxine (T4) are decreased, TSH levels are high in primary but may be normal in secondary
Improving oxygenation in hypothyroidism
monitor resp status; apply oxygen if needed; monitor lung sounds; use ventilator support if needed; sedation should be avoided unless necessary, and reduced dosage is required
Preventing hypotension in hypothyroidism
monitor BP, heart rate and rhythm, observe for signs of shock; report episodes of chest pain or chest discomfort; starting levothyroxine sodium at too high a dose or increasing the dose too rapidly can cause severe hypertension, heart failure, and myocardial infarct
Supporting cognition in hypothyroidism
observe and report lethargy, drowsiness, memory deficit, poor attention span, and difficulty communicating; problems should resolve within 2 wks of thyroid hormone replacement; orient pt and explain procedures; provide safe environment; encourage family to accept the mood changes and remind them that these problems should improve with therapy
Prevention of myxedema coma
at risk: acute illness, surgery, chemotherapy, discontinuing thyroid replacement therapy, use of sedatives or opioids
Emergency care of myxedema coma
patent airway; replace fluids with IV NS or hypertonic saline; give levothyroxine sodium; give glucose IV; give corticosteroids; check temp hourly; monitor BP hourly; cover pt with warm blankets; monitor for changes in mental status; turn pt every 2 hrs; institute aspiration precautions
Pt teaching for hypothyroidism
lifelong drug therapy; manifestations of hypo- and hyperthyroidism; medical alert bracelet; when to seek medical interventions; periodic blood tests; no OTC drugs (may interact with thyroid hormone prep); adequate fiber and fluid intake; take thyroid meds on empty stomach; resolution time varies; when pt needs more sleep and is constipated, dose should be increased; when pt has difficulty getting to sleep and has more BMs, the dose should be decreased
Adrenocorticotropic hormone (ACTH)
released by the pituitary; stimulates the release of cortisol, aldosterone, and androgen from the adrenal cortex
Vasopressin (antidiuretic hormone - AHD)
released by the posterior pituitary; promotes water reabsorption to maintain water balance
Thyroid stimulating hormone (TSH)
released by the anterior pituitary; stimulates the release of thyroxine (T4) and triiodothronine (T3) from the thyroid
