Study
Review All
Quiz!
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anterior lobe of pituitary secretes what growth hormones? |
prolactin, ACTH, TSH, FSH and LH |
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An altered stimulus to the anterior pituitary gland may produce what? |
one or multiple disorders |
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What are the 2 most common disorders of pituitary function? |
hypo and hyperpituitarism |
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What is Acromegaly? |
hypersecretion of growth hormone |
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When does acromegaly commonly occur? |
after epiphyseal closing during the young adult years |
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What is the most common cause of mortality from growth hormone deficiency? |
Cerebral Vascular Disease |
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What are the 4 main signs of Acromegaly? |
Cardiac diastolic function is impaired secondary to ventricular muscle hypertrophy, Sleep Apnea, peripheral neuropathy with muscular atrophy, neuropathic joints & other sequelae of nerve dysfunction |
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Acromegalic patients carry an increased risk of what? |
malignancy--colon cancer is the most likely associated type |
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What is the gold standard diagnostic test for Acromegaly? |
Oral Glucose tolerance test |
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In reference to an Oral Glucose tolerance test, Within 2 hours after ingestion of a 75-gram oral glucose solution, normal individuals supress their GH level to what number? |
less than 1 ug/L |
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What are the treatments for Acromegaly? |
transsphenoidal hypophysectomy to remove tumor, thyroid HRT, GH therapy, Radiation of the gland |
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What are the common side effects of GH therapy? |
fluid retention, arthralgia, and carpel tunnel syndrome ( they are usually dose related and improve with dose reduction) |
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What are the common side effects of Radiation of the gland? |
transient diabetes inspidus post op and increased urinary output |
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What is the list of clinical features in patients with Acromegaly? |
acral enlargement, arthralgias-neuropathic joints, carpel tunnel, coarsening of facial features, excessive sweating, goiter, hypertension-congestive heart failure, impaired glucose intolerance-diabetes, macroglossia, malocclusion and tooth gaps, pituitary mass effect including headache & visual field defects, partial/complete pituitary insufficiency, sensory & motor peripheral neuropathy, snoring &sleep apnea, sx r/t hyperprolactinemia, thick & course skin and skin tags |
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What are the subtle sx of GH deficiency in adults? |
decreased muscle strength & exercise tolerance, reduced sence of well-being |
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Patients with Adrenocorticotropic hormone (ACTH) deficiency are able to maintain what? |
mineralocorticoid secretion |
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What is Adrenocorticotropic hormone (ACTH) deficiency? |
a decreased or absent production of adrenocorticotropic hormone by the pituitary gland |
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What are the Sx associated with ACTH defficiency? |
chronic malaise, fatigue, anorexia, & hypoglycemia |
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With ACTH deficiency, why might an acute severe illness precipitate vascular collapse? |
cortisol is necessary for maintenace of peripheral vascular tone |
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Primary and Secondary adrenal insufficiency can lead to what? |
hyponatremia (this is secondary to inappropriate ADH secretion caused by cortisol defficiency) |
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The posterior lobe of the pituitary secretes what 3 things? |
ADH, Vasopressin, and oxytocin |
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What does vasopressin do? |
controls the reabsorption of free water |
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What are the 2 most common disorders of posterior pituitary function? |
diabetes & syndrome of inapropriate ADH |
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What is the etiology of Diabetes? |
deficiency of vasopressin causing post lobe dysfunction--lesions, CHI, CNS infections, brain tumor (cranial surgery) |
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What are the clinical manifestations of diabetes? |
polyuria (5-20 Liters Per Day), polydipsia, weight loss, dehydration, postural hypotension, & fatigue |
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What are the diagnostic tests for Diabetes? |
water deprivation test, a specific gravity less than 1.004, decrease NA & K+ levels |
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What is the tx for diabetes? |
IV solutions of glucose and saline, & vasopressin replacement |
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What is vasopressin? |
ADH |
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What 3 assesments are important for a patient with diabetes? |
BP, pulse, & respirations |
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What are 2 nursing goals for a patient with diabetes? |
stabilize fluid and electrolyte balance, & maintain fluid intake |
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What med intervention is appropriate for a diabetic patient as ordered? |
Desmopressin--a synthetic replacement for ADH |
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What is the etiology of SIADH? |
oversecretion of vasopressin |
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SIADH commonly occurs in what 5 things? |
neoplasms, nonmalignant pulmonary disorders, CNS disorders, AIDS, and drugs |
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What are the clinical manifestations of SIADH? |
decreased urinary output, increased body weight without edema, lethargy, headache, & cerebral edema |
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What are the diagnostic tests for SIADH? |
serium sodium > 134 mEq/l & a urine specific gravity > 1.005 |
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What is the treatment for SIADH? |
reduce fluid to 800-1000 ml q/day |
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What are important NSG assesments for a patient with SIADH? |
hourly I&O, daily weights, specific gravity, VS for low neurologic function, seizures, nausea, and vomiting |
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What are the NSG goals & interventions for a patient with SIADH? |
stabilize fluid and electrolyte balance, fluid restriction as ordered, mouth care, elevate head of bed no more than 5% to promote venous return, seizure precautions, administer IV fluids, diuretics and declomycin as ordered |
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What do the hormones of the thyroid gland do? |
stimulate cell metabolism |
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What is the main thyroid hormone? |
Thyroxin(T4)--a molecule that contains 4 iodine atoms |
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Which thyroid hormone is smaller but more potent than Thyroxin(T4)? |
Thiodothyronine(T3)--a molecule that contains 3 iodine atoms |
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What happens to cell metablism in a thyroxic state? |
it becomes accelerated & results in increased metablic rate, perspiration, O2 consumption by body cells, and rate of carbohydrate absorption |
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Cell metabolism is regulated by what? |
pituitary gland secretion of the thyroid stimulating hormone |
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Pituitary gland secretion increases and decreases with what? |
decreases: when T4 and T3 levels are high |
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Thyroid gland disorders are more common when and in who? |
when preexisting autoimmune disorders are present and in women |
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What is hyperthyroidism? |
hyperfunction of the thyroid that results from excess circulating levels of T3 and/or T4. |
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Hyperthyroidism is characterized by what state? |
hypermetablism |
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What are the 2 most common forms of hyperthyroidism? |
Graves disease & Multinodular goiter |
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What is graves disease? |
an autoimmune disorder in which antibodies attack thyroid tissue & stimulate hyperplasia |
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What is multinodular goiter? |
Benign or malignant nodules that autonomously secrete thyroid hormone |
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What are the goals of collaborative care for hyperthyroidism? |
to block the adverse effects of thyroid hormones & to stop their oversecretion with drugs, thyroid ablation with radiactive iodine, or surgical resection of the thyriod gland |
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What does the pituitary do in a state of hypermetablosism? |
supresses TSH to a point where it is low or undetectable |
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What do lab values, thyroid hormones, and thyroid stimulating hormones do in a state of Hyperthyroidism? |
Labs: Increase |
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What are the sx of Hyperthyroidism? |
nervousness, hand tremors, insomnia, tachycardia, cardiac dysrhythmia, weight loss(despite increased appetite), muscle weakness, increased sweating, heat intolerance, & increased peristalsis, goiter, exopthalmos(protruding eye balls), which can lead to mild to severe visual problems, high BMR, proximal muscle waisting, hpatomegally, deep tendon reflexes, decreased concentration, irritability/agitation, increased GI motility |
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What is the diagnostic test for detecting hyperthyroidism? |
TSH ASSAY (a screening test that detects even minimal thyroid hormone excess) |
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If a TSH Assay shows evidence that a patients TSH is less than normal what is performed next? |
a free T4 |
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What are the 3 treatments for hyperthyroidism? |
antithyroid drugs, ABLATION of a portion of the thyroid gland with Radioactive Iodine, & a thyroidectomy |
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Methimazole & propythiouracil are what type of drugs? |
antithyroid drugs for hyperthyroidism |
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What do antithyriod drugs do? |
concentrates in thyriod tissue, & blocks the synthesis of thyroid hormones causing a decrease autoimmune attack on the thyroid |
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What must be done when a patient is taking an antithyroid drug? |
monthly-follow ups, decrease meds as lab values return to normal, baseline lab data must include a leukocye count & liver function tests |
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What are possible side effects & adverse reactions of antithyroid drugs? |
agranulocytosis (decrease in leukocyes in the blood/bone marrow) not common and is reversible |
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A patient is instructed to discontinue take antithyriod medication & call MD if patient develops what sx? |
fever, sore throat and/or sore mouth, (sx of agranulocytosis), can also develop liver disease and a lupus-like syndrome |
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What is involved in the hyperthyroid tx: Ablation of the thyroid gland? |
Radioactive iodine PO is taken up by the thyroid gland which destoys some of the functioning thyroid cells that create T4. The therapeutic effects last 6-8 weeks. The majority eventually develop hypothyroidism & will need hormone replacement therapy for life. Don't give if pregnant. |
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What is involved in the hyperthyroid tx: Thyroidectomy? |
A change in voice will indicate injury to the vocal chords, ask pt to speak hourly post-op, inspect surgical dressing for bleeding (especially at the back of the neck), & change dressing as directed. Maintain seizure precautions, assess for: tetany, hoarseness, aphasia, & thyroid storm. Have tracheostomy tray and calcium gluconate available. Hypocalcemia is a potential surgical complication. Treat exopthalmos with prn eye drops. |
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What is a thyroid storm (thyroid crisis)? |
When thyroid blood levels reach life threatening levels . Will have exagerated sx of thyrotoxicosis and be in a hypermetabolic state. |
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When is a patient at greatest risk for a thyroid storm? |
within the first 4 years of dx of hyperthyroidism, it is usually and identifiable precipitating event ex. surgery, cessation of meds, DKA, CHF, pulmonary embolism, & high stress states |
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What are the signs of a thyroid storm? |
goiter, hyperreflexia, warm moist skin, muscle weakness, tachycardia, & systolic hypertension |
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What are the sx of a thyroid storm? |
nervousness, tremors, wekness, fatigue, confusion, delirium, or sometimes coma, palpitations, weight loss, high fever, dyspnea, and diarrhea |
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What is the medical management for a thyroid storm? |
treat cause to prevent reoccurence, increased/more frequent meds due to hypermetabolism (monitor electrolytes, VS, & thyroid function test), administer propranol to decrease HR and BP, acetiminophen to decrease fever, prevent vascular collapse, iv fluids to treat dehydration |
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Why would you not give ASA during a thyroid storm? |
it will increase binding capacity of T3 & T4 causing an increase in free thyroid hormone |
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WHat is the thyroid diet for a thyroid storm? |
high protein, carb and calorie, restrict stimulants like caffeine |
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What is "Lugol's solution" for a thyroid storm? |
reduce the size & vascularity of the thyroid gland |
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What is a major cause of hypothyroidism in adults? |
Hashimotos disease |
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What is Hashimotos disease? |
a chronic lymphocytic thyroiditis. The thyroid gland is unable to respond to the pituitary's thyroid stimulating hormone stimulus. Thyroid hormone levels decrease, TSH levels increase. |
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What are the sx of hypothyroidism? |
Early: enlarged thyroid, fatigue, weight gain, & difficulty concentrating |
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What are the diagnostic tests for hypothyroidism? |
the most sensitive test: TPOAb, |
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What is the name of a synthetic thyroid hormone given for hypothyroidism? |
levothyroxine |
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What is the tx for hypothyroidism? |
thyroid hormone replacement with a synthetic thyroid hormone. Will not have full effect for 10-14 days. Take at same time each day with 1 glass of water on empty stomach, dont take w/ calcium carbonate, maalox, or iron (iron binds with thyroid hormone & blocks absorption)-monitor closely with coumadin throxine increase its effects. |
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What are the NSG interventions for hypothyroidism? |
teach pt to notify MD for sx of intolerance (which are sx of hyperthyroidism), Manage constipation, through drinking adequate fluids, eating high fiber foods, and increasing activities, Tell MD if pregnant but dont discontinue drugs Diet: high fiber, high protein, low calorie, low calorie with increased fluid intake |
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What is a Myxedema Coma? |
rare & serious end-stage renal complication of progressive hypothyroidism. |
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What are the signs/symptoms of a Myxedema Coma? |
altered mental status, defective thermoregulation, generalized interstital edema, sallow skin, lethargy, reported memory impairment, signs of hypometabolic state (swollen tongue, edema, obesity, & sparse hair), bradycardia, hypotension, & hypothermia |
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A myxedema Coma is usually precipitated by what? |
an ilness or event such as an infection, trauma, exposure to cold, or abruptwithdrawal of thyroid hormone |
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Myxedema Coma is most common in who and when? |
in winter with a high mortality rate & in the elderly |
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What is the tx for Myxedema Coma? |
reverse hypothermia, increase cardiac output, and raise thyroid hormone |
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What are the NSG measures for a Myxedema Coma? |
monitor VS, LOC, I & O, & continuous cardiac monitoring |
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What is the function of the adrenal gland? |
They are responsible for regulating the stress response through the synthesis of corticosteroids and catecholamines, including cortisol and adrenaline |
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What is pheochromocytoma? |
hyperfunctioning of the adrenal medulla |
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What is the cause of pheochromocytoma? |
catecholamine-secreting(epinephrine, norepinephrine) neoplasm. An increase in catacholamines cause hypertension, increased BMR & hyperglycemia |
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What are the signs/sx of pheochromocytoma? |
labile malignangt hyperternsion, and throbbing H/A, norepinephrine crisis (similiar to pannick attack), increased HR & BP, sweating, & angina. |
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What is this diagnostic for pheochromocytoma? |
through urine collection and test for increased VMA (Vanillylmandelic acid) |
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What are the interventions for pheochromocytoma? |
high calorie diet, increase in vitamins and minerals, estrict stimulants, semi fowlers position, monitor BP, urine glucose & ketones daily |
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WHat are the medical treatments for pheochromocytoma? |
regitine, alpha adrenergic blockers, & vasodilators |
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What are the possible complications of pheochromocytoma? |
can cause cardiac arrest, cerebral hemmorhage blindness and renal failure |
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What are the sx for Cushings syndrome? |
hirsutism, glycosuria, leukocytosis, polycthemia, hypercalcuria, hypercoagulability, HTN w/ hypervolemia, thin fragile skin abdominal striae, edema, truncal obesity, moon face (caused by fat redistribution), buffalo hump,inhibition of immune & inflammator Response, mood swings, muscle waisting, amenorrhea, gynecomastia, joint pain, reoccurent infection |
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Cushing's Syndrome can lead to what? |
Type II DM |
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What is th Dx tests for Cushings Syndrome? |
1. Single Best test: 24 hour urinary free cortisl meaurement |
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What are the tx for Cushings syndrome? |
Meds: antidiabetic for hyperglycemia, adrenal suppresants, Surgery: adrenalectomy or hypophysphectomy, Diet: low NA, carb, kc & high K+ & protein |
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What are the NSG interventions for Cushings Syndrome? |
assess for adema, I&O, daily weights, fluid restriction, protect from infections, provide rest periods |
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What is an adrenalectomy? |
removal of one or both adrenal glands, this surgery disturbs mineralcorticoid and glucocorticoid secretion causing altered fluid & electrolyte balance, keep pt in semi-fowlers, maintain quiet environment, need for life long med replacement, replacement meds start preop to prepare for the sudden drop |
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What is a hypophysectomy? |
removal of part or all of the pituitary gland |
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What is involved with a hypophysectomy? |
PO care, monitor for ICP, assess cardiac, respiratory, and neurologic status and fluid balance, inspect surgical dressing or nasal drip pad & chage prn, keep pt in semi fowlers, check for rhinorrhea, avoid coughing, blowing nose, lifting, straining, & comply with lifelong hormone replacement |
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What are 2 possible post op comp. of Cushings syndrome? |
thyroid storm and adrenal crisis from a deficiency of mineralcorticoids & glucocorticoids. It usually follows acute stress, sepsis, trauma, surgery or omission of steroid therapy. it's a medical emergency, tx: hydrocortisone with 3-5 ml of saline solution |
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What is addisons Disease? |
adrenal hypofunction, insufficient secretion of mineralcorticoids: |
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What are the sx of Addisons Disease? |
severe hypotension, orthostatic hypotension, hyperkalemia, hypoglycemia, weakness lethargy, weight loss, hyperpigmentation (bronzed skin, high pigmentation of nipples, scars & buccal mucosa), alopecia, low axillary and pubic hair in women, anemia, lymphocytosis, insulin sensitivity, propensity toward autoimmune diseases, cramping, ab pain, diarrhea, neurasthenia & depression, salt craving |
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What are the physiological effects of Addisons Disease? |
1. low aldosterone-causes disturbances in NA, H20, & K+ metablism |
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What are the dx tests for Addisons? |
1. morning cortisol level <5>15=rules it out |
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What is the NSG management for Addisons disease? |
replacement therapy, diet: high car, protein, NA, Low K+ in small frequent feedings before steroid therapy. High K+ low NA when on steroid replacement therapy. Maintain hydration to prevent addisons crisis, avoid strenous exercise-especially in hot weather, increase fluids in hot weather & carry injectable dexamethasone. |
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What is the potential comp. of Addison's disease? |
Addisons Crisis: sx=hypotension, cyanosis, ab cramps, diarrhea, costovertabral tenderness, fever, confusion, coma |
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What is the tx for addisons crisis? |
admin. IV hydrocortisone, & saline solution to reverse shock, hyponatremia |
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What can a sudden increase/decrease of steroids cause? |
Increase=weight gain |
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What does the parathyroid gland secrete & what is its function? |
it secretes parathyroid hormone & it stimulates the bones, kidneys, & intestines to increase blood calcium levels. |
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What is hyperparathyroidism? |
excessive secretion of PTH which leads to bone demineralization. |
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What are the sx of hyperparathyroidism and what are they r/t? |
r/t hypercalcemia because of the severity and rate of change of the serium calcium, "bones, stones, and ab moans", constipation, ab pain, anorexia, muscle weakness, aches, pains, polyuria, nocturia, polydipsia, H/A, fatigue, cognitive dysfunction, shortened QT interval, PC fractures, renal calculi, arythmias |
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What are the dx tests for hyperparathyroidism? |
EKG, High parathyroid hormone and high Ca+(3.5-5=norm), Urinary calcium excretion is measured by 24 hour urine collection that will specify total volume & urine creatinine levels, family hx, ultra sound, visualization of the glands |
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What is the NSG Management for hyperparathyroidism? |
Diet: low Ca+ (norm=3.5-5), high fiber, high phos in small frequent feedings, increase fluids to 3000 ml/day, encourage acidifying fluids like cranberry juice because of risk for stones, LAB studies: Ca+, phos, BUN, creatinine, K+, Na+. Surgical removal of glands if pt under 50 & has hx of comp. ex. hypercalcium crisis, overt bone disease, nephrolithiasis |
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What is hypoparathyroidsim? |
a decrease in parathyroid secretion. low stimulation to osteoclasts, resulting in a decreased release of ionized Ca+ (<4.4) & phos from bone. There is a decreased GI absorption of Ca+ and increased absorption of phos. Low blood Ca+ causes a rise in serium phosphates & decreased phosphate excretion by the kidneys. |
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What are the sx of hypoparathyroidism? |
neuromuscular irritability, tetany(repetitive neuromuscular discharge after a single stimulus), hypocalcemia, deep tendon reflexes, paresthesias in circumoral & sacral areas, fingers, and toes, + chovestek's sign-twitching of the face by tapping over cranial nerve VII at the ear, + Trousseaus sign(inflation of the BP cuff can result in carpal smasm), CV sx: increased QT wave, CHF, hypotension, Autonomic sx: bronchial spasms, stridor, diaphoresis, Neuropsychiatric sx: seizures, dementia, mental retardation (in children), emotional problems (anxiety, depression) extrapyramidal sx: parkinsons is the most common, pappiledema |
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What is the Tx for hypoparathyroidism? |
Ca+ and vit D supplements, phos levels should also be controlled. If phos is >6 at a time when Ca+ is satisfactory, an unabsorbable phosphate binder should be added to the regimen, a synthetic PTH preperation SQ BID, Diet: high calcium, low phos, low Na+ w/ spinache restriction. Keep trach tray & IV Ca+ gluconate available |
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What is the function of the Kidney? |
excretion, absorbtion, & regulation, |
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What are the r/f for Renal Disease? |
over age of 65, black, native americans, maj of ESRD pts dx with DM or HTN |
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What is chronic Renal Failure? |
also known as ESRD, occurs when there is a progressive & irreversible reduction in the kidneys ability to remove waist & maintain homeostasis |
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What is uremic syndrome |
sx are caused by kidney's inability to perform excretory(elimination of urea, creatinine, uric acid), secretory (renin, erythropoietin, prostoglandins & active metabolite of vit D) & regulatory functions (level of extracellular fluid volume, osmolarity, electrolye balance, & acid-base balance) that results in the disruption of homeostasis. Effects all organs. |
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What are the effects of chronic renal failure? |
listed on page 7 in regulatory mechanisms |
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What is the NSG management for chronic renal failure? |
monitor diet (renal diet-protein & electrolyte restrictions, certain # of calories & specified mineral & vit. requirements), protein restriction to decrease nitrogenous waste accumulation from protein metablism, intake of sufficient carbs & fats promits protein sparing, control of K+ & Na+ based on kidney function to prevent hyperkalemia (cardiac dysrhythmias) & hypernatremia (edema & hypertension), restriction of phos to prevent renal bone disease, restrict fluids to 500cc + urinary output or 1000cc w/ dialysis may not be restricted w/ peritoneal dyalysis, I&), dail weights, manage thirst, monitor labs:electrolyes, CBC, BUN, Creatinine, teach pt's family complications (infection, bleeding, electrolyte imbalance) disease procress, not to use OTC meds because many have K+,& how to measure I&O |
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What is acute renal failure? |
develops over a period of a few hours to several days in response to a loss of kidney function, clients manifest a progressive retention of nitrogenous wastes (azotemia) as seen in an elevation of BUN & renal tissue damage as indicated by elevated serum creatinine levels. It is progressive & irreversible. There are 3 categories with 3 distinct phases. |
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What are the 3 categories of acute renal failure? |
1. prerenal |
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What is involved in the prerenal category of acute renal failure? |
hypoperfusion of the kidneys without permanent injury to them. Etiology: burns, cardiogenic abnormalities, diarrhea, hemorrhage, intervascular hemolysis, intestinal obstruction, sepsis, & vomiting |
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What is involved in the intrarenal category of acute renal failure? |
permanent damage to the kidneys through infectious, immunologic or vascular disease processes, prolonged ischemia or nephrotoxic are also causes of internal ARF. |
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What is involved in the postrenal category of acute renal failure? |
A mechanical obstruction in the urinary collection system at any point (bilateral uretic, bladder, prostatic or urethral) which causes the back up of urine into the renal pelvis . Etiology of the obstruction may be blood clots, calculi, benign prostatic hyperplasia, neoplasms and trauma. |
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What are the 3 distinct phases of acute renal failure? |
1. oliguric 2. diuretic 3. recovery |
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What is involved in the oliguric phase of ARF? |
1-7 days after event, high bun creatinine, urine output=<400ml/24 hrs., S.G. 1.010-1.016, proteinuria, acidosis, hyperk+, hypercal, pulm. edema, kussmauls resp., pleural effusion, fluid volume excess can lead to CHF, hypertension, pericardial effusion, cardiac dysrythmias, anorexia, vomiting, diarrhea, constipation, lethargy progressing to disorientation and coma, anemia, leukocytosis, decreased skin turgor, pruritus, dry mucosa |
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What is involved in the diuretic phase of ARF? |
1-3 weeks dramatic increase in urine output, gradual decrease of BUN & Creatinine, 4-5 L of urine output/day, <1.010, positive/negative proteinuria, hypoK+, hypocal, hypoNa+, hypotension, tachycardia, improved LOC, fluid volume deficit can lead to hypovolemic shock as the CO decreases |
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What is involved in the recovery phase of ARF? |
lasts 1-2 years, everything has returned to normal and BUN is stable |
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What are important things to monitor for in both the oliguric & diuretic phase? |
monitoring of serum, & monitoring potassium is crucial to prevent arrythmias, and multisysem complications |
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NSG management for ARF is? |
directed at restoration of renal function and/or prevention of further damage to kidney function |
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What are important NSG assesments for ARF? |
vitals, I&O/hourly, urine specific gravity, urine for protein, hematuria, casts, daily weight for fluid retention, LABS: BUN, creatinine, electrolytes, ABG's & CBC, bleeding time |
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Clients that are unresponsive to coneventional therapy for ARF become candidates for what tx? |
dialysis |
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What is the purpose of dialysis? |
to restore normal fluid environment, remove waste products of metabolism, correct acid base balance, electrolyte concentration, and replenish bicarb buffer system. |
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Peritoneal dialysis increases risk for what? |
hyperglycemia |
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What are the causes of renal calculi? |
a diet high in Ca+, vit D, milk, protein, oxalate, or alkali, gout, hyperthyroidism, UTI, dehydration, & hypercalcemia |
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What are the signs & Sx of renal calculi? |
flank pain, renal colic, costovertebral tenderness, frequency & urgency of urination |
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What is the dx test for renal calculi? |
intravenous pylegram |
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How does the intravenous pyelegram work? |
assess for allery to shellfish or iodine, radiopaque material is given IV. Multiple radiographs of the urinary tract are taken while the material is excreted providing important info. about the structure and function of the kidney, ureter and bladder |
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What diet should be followed when a pt has renal calculi? |
calcium stones (acid-ash)= limit calcium intake |
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What is the tx for renal calculi? |
extracorporeal shock wave lithotripsy, increase fluid intake, moist heat to flank, hot baths |
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What is nephrosis? |
A condition in which there are degenerative changes in the kidneys, especially the renal tubules, without the occurence of inflammation. Protein loss is so extensive that edema and proteinemia are produced. |
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What is acute glomerulonephritis? |
inflammation of the capillary loops in the glomeruli of the kidney |
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What is acute glomerulonephritis caused by? |
strep infection of the resp. tract, or a skin infection like impetigo |
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What are the signs/sx of acute glomerulonephritis? |
peripheral & periorbital edema, tea-colored urine, elevated temperature, flank pain, & oliguria |
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What are the dx test for acute glomerulonephritis? |
urinalysis reveals proteinuria & hematuria. RBC's, WBC's, & mixed cell casts are common findings in urinary sediment |
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What is the recommended diet for acute glomerulonephritis? |
high carbs, & high vit.'s with restricted intake of Na+, protein, K+ and fluids |
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1.What is nephrotic syndrome? |
1. the end result of a variety of diseases that damage the cappilaries of the glomerulus. This leads to the loss of a large amount of protein in the urine, hypoalbuminemia, and edema. |
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1. What is hydronephrosis? |
1. a collection of urine in the renal pelvis from obstructed outflow, forming a cyst by production of distention and atrophy of the organ. |
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Nephrotic syndrome is characterized by what sx that result from changes that occur to small functional structures in the kidneys? |
high levels of protein in the urine, low levels of protein in blood due to its loss in the urine, whole body edema, ascites in abdomen, high cholesterol levels in the blood |
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1. WHat type of nephrotic syndrome is most common in children? |
1. ideopathic nephrotic syndrome |
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What is the most common type of ideopathic nephrotic syndrome? |
minimal-change nephrotic syndrome |
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Minimal change nephrotic syndrome |
child usually has relapses of the ilness, but the disease can usually be managed and prognosis is good. In rare cases a child may develop kidney failure that requires dialysis |
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Common sx of nephrotic syndrome include what? |
fatigue & malaise, decreased appetite, weight gain & facial swelling, ab swelling or pain, foamy urine, fluid accumulation in body spaces (edema), pale fingernail beds, dull hair, ears and cartilage may feel less firm, food intolerances or allergies |
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What is congenital nephrotic syndrome? |
rare, 1st week of life, inherited by autosomal recessive gene-means that males & females are equally affected, & the child inherited one copy of the gene from each parent, who are carriers, the chance for carrier parents to have a child with nephrotic syndrome is 1/4 with each pregnancy, the outcome for this type of nephrotic syndrome is very poor. |
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How is nephrotic syndrome diagnosed? |
physical exam, med history, urine test to check for protein, blood test to check levels of cholesterol and a special blood protein called albumin, renal ultrasound-a non invasive test in which a transducer is passes over the kidney producing sound waves which bounce off the kidney, transmitting a picture of the organ on a video screen . The test is used to determine the size and shape of the kidney, & to dect a mass, kidney stone, cyst, or other obstruction or abnormalities, renal biopsy-(a procedure where a small sample of tissue is taken from the kidney through a needle ,the tissue is sent for special testing to determine the specific disease |
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Kinds of treatment used for nephrotic syndrome depends on which factors? |
childs age, overall health, and medical history, extent of the disease, childs tolerance for specific meds, procedures, or therapies, expectations for the course of the disease, your opinion/preference |
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What happens during the initial episode of nephrotic syndrome? |
child may require hospitilazation, may need to be monitored if edema is severe, if child has BP and/or breathing problems |
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What meds are used to tx nephrotic syndrome? |
immunosuppresive drug therapy, diuretics(to reduce edema), IV albumin- ablood protein that can be administered to rplace the low levels, & a special diet that restricts salt and has other spec. |
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Why should a child not receive live vaccines when receiving mephrotic syndrome meds? |
because the meds weaken the immune system, however, if child has been exposed to chicken pox & hasnt had the vaccine, the vaccine may still be reccommended |
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What is the long term outlook for nephrotic syndrome? |
relapses do occur throughout childhood. however, once a child reaches puberty, the disease usually stays in remission, its uncommon for sx to return during adulthood however it is possible. |
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What does the pituitary gland do? |
repsonds to signals from the hypothalmus. It releases hormones, some of which control other endocrine glands. |
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What does the pararthyroid gland do? |
They are 4 patches of tissue on the thyroid gland that release the parathyroid hormone which regulate the blood clacium level |
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WHat does the thymus do? |
thymosin, which stimulates the development of T cells for the immune system is secreted by the thymus. |
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What does the Adrenal glands do? |
they make epinephrine & norepinephrine, 2 hormones which cause the fight or flight respons. They also secrete aldosterone which affects the bodies osmotic balance and cortisol which promotes glucose synthesis |
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What do the testes do? |
make testosterine, a hormone that maintains the male reproductive system and secondary sex characteristics |
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What do the ovaries do? |
the hormones estrogen and progesterone are made here. they maintain the female reproductive system and secondary sex characteristics. Progesterone maintains the uterus during pregnancy |
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What is a goiter? |
an enlarged thyroid gland, may be diffuse or nodular, it may extend into the retrosternal space, with or without substantial anterior enlargement, because of the anatomical relationship of the thyroid gland to the trachea, larynx, superior and inferior laryngeal nerves, and esophagus, abnormal growth may cause a variety of compressive syndromes. Thyroid function may be normal (nontoxic goiter), overactive(toxic goiter, or underactive(hypothyroid goiter) |
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What is the patho of a goiter? |
the thyroid gland is controlled by the thyrotropin, secreted from the pituitary gland, ehich in turn is influenced by the thyrotropin-releasing hormone from the hypothalmus. TSH permits growth, cellular differientation, & throid hormone production and secretion by the thyroid gland. Thyrotropin acts on TSH receptors located on the thyroid gland. Serum thyroid hormones levothyroxine & triiodothyronine feedback to the pituitary, regulating TSH production. Interference with this TRH-TSH thyroid hormone axis causes changes in the function and structure of the thyroid gland. Stimulation of the TSH receptors of the thyroid by TSH, TSH receptor antibodies or TSH receptor agonists, such as chorionic gonadotropin, may result in a diffuse goiter. When a small group of thyroid cells, inflammatory cells, or malignant cells metastatic to the thyroid is involved, a thyroid nodule may develop |
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What is the patho of a goiter-continued |
A deficiency in thyroid hormone synthesis or intake leads to increased TSH production. |
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What are the 2 types of goiters and definitions? |
1.toxic goiter-associated w/ hyperthyroidism. Ex. diffuse toxic goiter(graves disease), toxic multinodular goiter, and toxic adenoma (plummer disease) |
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What are the etiologys for goiter? |
iodine defficiency, autoimmune thyroiditis: hashimotos or postpartum thyroiditis, excessive iodine (wolff-chaikoff effect) or lithium ingestion with decreased release of thyroid hormone , goitrogens, stimulation of TSH receptors by TSH from pituitary tumors, pituitary throid hormone resistance , gonadotropins, and or thyroid stimulating immunoglobins, inborn errors of metablism causing defects in biosynthesis of thyroid hormones, exposure to radiation, deposition diseases, thyroid hormone resistance, subacute thyroiditis(de quervain), silent thyroiditis, riedel thyroiditis, infectious agents-acute suppurative:bacterial, chronic:mycobacteria, fungal, and parasitic, granulomatous disease, thyroid malignancy |
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What is the tx for goiters? |
iodine supplementation, or levothyroxine may reduce goiter size (thyroid hormone). The most widely used thyroid hormone is levothyroxine sodium, admin. once/daily |
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Description of levothyroxine sodium if need to know? |
page 15 of regulatory mechanisms |
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Care Plan for hyperthyroidism may need to be reviewed |
no flash cards were created for care plan:pg 16-23 of Regulatory Mechanisms |
