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endocrine
| Term | Definition |
|---|---|
| ADH | DI SIADH |
| DI | ADH Deficiency, dehydration |
| clinical manifestations of DI | increased urine output, dilute, weight loss, dehydration, hypernatremia-thirst, dry mucous membranes, hypotension, increase in serum osmorality, decrease in urine osmorality |
| Interventions for DI | I&O weights, increase fluids, monitor therapy, home care-weights, increase sodium, decrease urine specific gravity |
| Medication for DI | Desmopressin, vasopressin-educate patient if polyuria or polydipsia take more medication, daily weights, medical alert bracelet, keep meds and water bottle at all times |
| SIADH | ADH inapporpriate, fluid volume retention |
| Clinical manifestations of SIADH | decreased urine output, concentrated, weight gain without edema, hyponatremia-confusion, ha, seizures, decreased serum osmolality, increase in urine osmorality |
| Interventions of SIADH | fluid restriction, I&O, monitor therapy, seiure precautions, decrease environmental stimuli, monitor fluid overload. |
| Medication for SIADH | Tolvaptin, 3% sodium IV solution, dieuretics |
| Labs for SIADH | decreased Na<135, serum osmolality decreased <275, urine osmorality increased >100, urine specific gravity increased >1.030 |
| Labs for DI | increased Na>145, serum osmolality increased >295, decreased urine osmorality<100, decreased urine osmorality<1.005 |
| Nursing considerations for SIADH | monitor fluid status, I&O, daily weights, monitor Neuro checks, risk for seizures, fluid restriction and mouth care |
| Nursing considerations for DI | monitor urine output and specific gravity, replace fluids and monitor for dehydration, assess for signs of shock-hypotension, tachycardia |
| Causes for SIADH | CNS disorde4rs-head injury, stroke, brain tumor, meningitis, cancers, drugsSSRI's pulmonary disorders-pneumonia, TB |
| Causes for DI | central DI-head trauma, pituitary surgery, tumor, idiopathic. Nephrogenic DI-renal disease, lithium, demeclocycline, hypercalcemia, hypokalemia. |
| Hypothyroidism | decreased thyroid hormone production-slowed metabolism, under active thyroid |
| Hyperthyroidism | increased thyroid hormone production,-accelerated metabolism, overactive thyroid |
| Clinical manifestations of hypothyroidism | fatigue, weight gain, cold intolerance, bradycardia, hypotension, dry, course skin, constipation, slow speech, irregular menses, Myxedema coma |
| Clinical manifestations of hyperthyroidism | restlessness, weight loss, heat intolerance, tachycardia, hypertension, warm moist skin, diarrhea, nervousness, amenorrhea,decreased fertility, Thyroid storm |
| Labs for Hypothyroidism | decreased T3 and T4, increased TSH, RAIU low. |
| Labs for hyperthyroidism | increased T3 and T4, decreased TSH RAIU high especially in graves disease |
| Treatment for hypothyroidism | synthroid Levothyroxine, lifelong therapy, take on empty stomach, avoid sedatives and narcotics, monitor for hyperthyroid symptoms from overmedicated. |
| Treatment for hyperthyroidism | antithyroid drugs-methimazole and PTU propylthiouracil, beta blockers-propranolol for tachycardia, radioactive iodine therapy, thyroidectomy if unresponsive to meds |
| Nursing care for hypothyroidism | monitor for bradycardia, hypotension and resp depression, encourage warm environment, educate medication for synthroid, monitor TSH levels regularly |
| Nursing care for hyperthyroidism | montitor for thyroid storm-fever, tachycarida, hypertension, restlessness, provide cool environment, reduce stimulation, evncourage high calorie diet, |
| Myxedema coma | triggered by infection, surgery, or stopping meds, hypothermia, bradycardia, hypotension, hypoventilation, IV thyroid hormone, warming and airway support |
| Thyroid storm | triggered by infection, surgery, trauma, or stress, high fever, tachycardia, hyptertensnion, agitation, delirium, beta blocker, antithyroid meds, cooling, IV fluids. TEMP 1 degree change. |
| Thyroidectomy | Monitor airway, check for bleeding, keep trach tray at bedside, monitor for hypocalcemia(chvosteks and trousseau's sign) |
| Hyperparathyroidism | Excess PTH secretion-increased calcium, and decreased phosphorus, hypercalcemia>10.5, osteoporosis |
| Hypoparathyroidism | deficient PTH-decreased calcium and increased phosphorus, hypocalcemia<8.5, neuromuscular excitability, tetany |
| Primary cause of hyperparathyroidism | parathyroid adenoma or hyperplacia |
| Secondary cause of hyperparathyroidism | CKD, vit d deficiency |
| common cause for hypoparathyroidism | accidental removal, damageduring thyroid or neck surgery, autoimmune destruction, and hypomagnesemia |
| clinical manifestations for hyperparathyroidism | fatigue, depression, kidney stones, and pain, constipation, bone pain/fx, polyruia, dehydration, N/V, bone deminieralization |
| clinical manifestations for hypoparathyroidism | tetany, muscle cramps, tingling lips/fingers, pos chvosteks and trousseau's signs, anxiety, dry brittle nails, cataracts. |
| Nursing plan for hyperparathyroidism | lower ca levels, protect bones, hydration prevent kidney stones, |
| Medications for hyperparathyroidism | calcimimetics cinacalcet, decreased PTH secretion, bisophonates alendronate, decreased bone loss, Loop diuretics furosemide, increased ca secretion. |
| nursing care for hypoparathyroidism | raise ca levels, replace PTH effect, magnesium replacement-high calcium, low phorphate diet avoid dairy will increase |
| Medications for hypoparathyroidism | calcium supplements IV calcium gluconate for a cute tetany, vitamin d calcitriol, enhance ca absorption, mag replacement if low |
| Complications for hyperparathyroidism | kidney stones, osteoporosis, fx, cardiac dysrhthmias |
| complications for hypoparathyroidism | laryngospasms, airway, obstruction, seizures, cardiac arrhythmias. |
| Addison's disease | decreased cortisol, decreased aldosterone, stress tolerance, hypoglycemia, lack of aldosterone-sodium loss, potassium retention-dehydration and hypotension. ACTH increased causes hyperpigmentation |
| Cushings syndrome | excess cortisol, hyperglycemia, protein breakdown, excess aldosterone-sodium retention, potassium loss-hypertension, fluid overload, increased cortisol suppresses ACTH-thin skin, striae, immunosuppression |
| Clinical manifestations of addisons | bronze skin, weight loss, fatigue, hypotension, orthostatic, decreased Na, and glucose, increased K, N/V/D, amenorrhea, depression, Shock |
| Clinical manifestations of cushings | Moon face, buffalo hump, weight gain, thin fragile skin, muscle weakness, hypertension, increased Na, and glucose, decreased K, fluid retention, increased appetite, acne, irritability, Severe infection,HF, Hyperglycemia |
| Complications for addisons | stress, infection, trauma, abrupt steroid withdrawal, Severe hypotension, shock hypoglycemia, and hyperkalemia |
| Complications for cushings | infection, trauma, abrupt stopping of steroids, extreme Hyperglycemia, Severe HTN, psychosis |
| Medications for addisons | lifelong hormone replacement-prednisone-increase dose during stress, avoid abrupt withdrawal, diet increase Na, fluids, decreased potassium, wear medical alert bracelet |
| Medications for cushings, | gradual taper of corticosteroids, aminoglutethimid-blocks cortisol synthesis. DIet low Na, High K and potassium. prevent infection |
| Addison=ADD | Need to replace hormones |
| Cushings=cushy | too much cushion for horomones need to decrease |
| PHeochromocytoma | rare catecholamine secreting tumor, usually benign, causes excess production of epinephrine and norepinephrine |
| Symptoms of pheochromocytoma | h/a heart, heat. |
| Complications of pheochromocytoma | hypertensive crisis-stroke, MI, HF. cardiac arrhythmias, shock post surgery. |
| Pre-op for pheocromocytoma | alpha blockers-phenooxybenzamine or doxazosin for 7-14 days-control b/p and prevent crisis. Beta blockers-propranolol-after alpha blockade to control tachycardia. |
| Post-op for pheocromocytoma | monitor for hypotension, shock, or hypoglycemia, lifelong f/u for recurrence or endocrine tumors. |
| Priorities for pheocromocytoma | monitor bp and hr closely, avoid palpating the abdomen, maintain calm quiet environment |
| PHEO | pressure high from excess catecholamines outburst |
| HHS-hyperosmolar hyperglycemic state | Type 2, gradual, some insulin-enough to prevent ketosis but not enough to prevent Hyperglycemia, no ketosis, leads to severe dehydration |
| DKA-diabetic ketoacidosis | Type 1, rapid onset, no insulin-cells can't use glucose, body breaks down fat-ketone buildup, metabolic acidosis, leads to K loss, dehydration. |
| Clinical manifestations of DKA | blood glucose>250, +ketones, osmolality<320, polyuria, kussmaul respiration-deep rapid, fruity breath, K is initially high but drops with treatment |
| Clinical manifestations of HHS | blood glucose>600, no ketones, osmolality>320, polyuria, normal or shallow breathing. |
| Priority for DKA | fluids-NS then switch to 0.45% NS if Na is high, insulin therapy, replace potassium if under 5, treat casue- infection MI, add dextrose 5% when glucose is <200. |
| Priority for HHS | fluids-NS then switch to 0.45%, insulin therapy, replace potassium as needed, add 5% dextrose if under 300 |
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