Studied by 8 peoplecorticotrophin-releasing hormone, thyrotropin-releasing hormone, growth hormone-releasing hormone, gonadotropin-releasing hormone, prolactin-releasing factor
what hormones are released by the hypothalamus?
antidiuretic hormone, oxytocin
what hormones are released by the posterior pituitary gland?
growth hormone, adrenocorticotropic hormone, thyroid stimulating hormone, gonadotropic hormone
what hormones are released by the anterior pituitary?
T3 and T4, calcitonin
what does the thyroid release?
metabolic rate, oxygen consumption, carbohydrate/lipid metabolism, growth/development, brain function
functions of the thyroid gland include -
iodine
what is required by the thyroid to produce T3 and T4
calcitonin
lowers serum calcium levels -
inhibiting transfer of calcium from bone to blood; increasing calcium storage in bone; increasing renal excretion of calcium and phosphorus
how does calcitonin lower serum calcium levels?
women
who is more likely to develop Graves’ disease?
thyrotoxicosis
physiologic effects/clinical syndrome of hypometabolism; results from increasing circulating levels of T3, T4 or both
Radioactive iodine uptake (RAIU)
used to differentiate Graves’s disease from other hyperthyroid syndromes
de3crease tachycardia, nervousness, irritability, tremors
what symptoms does beta blockers treat in hyperthyroidism?
propranolol (inderal)
what beta blocker is used to treat hyperthyroidism?
atenolol
what beta blocker is indicated in a patient with asthma or heart disease when treating hyperthyroidism?
pregnancy
what is a contradiction of radioactive iodine therapy?
high incidence of hypothyroidism following treatment; need for lifelong thyroid hormone replacement
what is the disadvantage of radioactive iodine therapy?
three months
how long will it take for radioactive iodine therapy take to have effects?
antithyroid drugs and beta blockers
how is hyperthyroidism treated before radioactive iodine therapy shows effectiveness?
thyroid storm
life-threatening condition that occurs with release of excessive amounts of thyroid hormones; all symptoms of hyperthyroidism are heightened
a stressors (infection, trauma, surgery)
what causes a individual to go into thyroid storm?
hyperthermia, restlessness, N/V/D, severe tachycardia, delirium/coma
what are some s/s of thyroid storm?
reduce fever
what is the main goal when treating an individual with thyrotoxicosis?
cardiac monitoring (arrhythmias), oxygen therapy, IV fluid administration, calm environment, protect eyes
nursing considerations associated with thyrotoxicosis include -
subtotal thyroidectomy
removal of significant portion of thyroid
90%
how much of the thyroid needs to be removed during a subtotal thyroidectomy for it to be effective?
unresponsive to drug therapy, large goiter causing tracheal compression, thyroid cancer, not a candidate for RAI
what are some indications for subtotal thyroidectomy?
observe for tetany (due to hypocalcemia) and laryngeal stridor
which presentation following a thyroidectomy would be most concerning?
trousseau’s sign
carpal spasm, induced by blood pressure cuff applied and inflated
chvostek’s sign
contraction of facial muscles following stimulation
low calcium (have calcium bedside)
what do trousseau’s sign and chvostek’s signs indicate in the patient post thyroidectomy?
reduce caloric intake, avoid goitrogens, adequate iodine intake, avoid high temperatures
patient teaching following a subtotal thyroidectomy includes -
it will inhibit the production of TSH by the pituitary
why is thyroid hormone not prescribed following a subtotal thyroidectomy?
goitrogens
foods or drugs that contain thyroid inhibiting substances
lack of iodine, over/underproduction of thyroid hormones, thyroiditis
what are possible causes of goiters?
primary hypothyroidism
destruction of thyroid or defective T3/T4 synthesis
secondary thyroiditis
pituitary or hypothalamus dysfunction
hashimoto’s thyroiditis
chronic autoimmune thyroiditis; destruction of thyroid tissue by antibodies
goiter
what is a hallmark sign of Hashimoto’s thyroiditis?
low T3 and T4 and high TSH
what do labs for Hashimoto’s thyroiditis look like?
decreased HR/contractility, dyspnea upon exertion, slowed mental status, weight gain, puffy face, cold intolerance
s/s of hypothyroidism
decreased rate and contractility; tendency to develop CHF, angina, and MI
what are important cardiac complications of hypothyroidism?
dyspnea on exertion
what are important respiratory symptoms associated with hypothyroidism
apathy, lethargy, slowed mental status
hallmark neural signs of hypothyroidism include -
weight gain, constipation
hallmark GI signs of hypothyroidism
prolonged menstrual periods or amenorrhea
hallmark reproductive sign of hypothyroidism
levothyroxine
what is the choice drug used to treat hypothyroidism?
low calorie diet
what is a lifestyle change recommend for hypothyroid patients?
slow - angina (sudden increase of oxygen from the heart)
how should you start hypothyroidism treatment in older adults? why?
myxedema coma
life-threatening complication associated with hypothyroidism; lethargy and mental impairment progress into coma
infection, drugs, cold
what are factors that could cause myxedema coma?
subnormal temperature, hypotension, hypoventilation, hypoglycemia/hyponatremia, CV collapse
s/s associated with myxedmea
antidepressants, digitalis compounds, anticoagulants
what drugs will thyroid medications potentiate?
avoid enemas (vagal stimulation)
what should patients with hypothyroidism avoid when treating their constipation?
calcium an phosphate
the parathyroid gland controls levels of what?
primary hyperparathyroidism
increase in PTH due to benign neoplasm
lithium therapy
what is the treatment for primary hyperparathyroidism?
radiation to head and neck
what increases the risk for primary hyperparathyroidism?
secondary hyperparathyroidism
compensatory response to any state that causes hypocalcemia
vitamin D deficiency, malabsorption, chronic kidney disease, hyperphosphatemia
what are possible causes of hyperparathyroidism?
tertiary hyperparathyroidism
hyperplasia of glands; loss of negative feedback; autonomous secretion - NORMAL CA LEVELS
greater than 10mg/dl
what serum Ca would be indicative of hyperparathyroidism
less than 3mg/dl
what serum phosphate is expected in hyperparathyroidism?
surgery
what is the most effective treatment for hyperparathyroidism
transport normal tissues or take Ca supplementation for life
how is the calcium level handled during surgery treatment of hyperparathyroidism?
elderly
what is a reason a patient with hyperparathyroidism would not receive surgery?
IV NaCl and loop diuretics; biphosphates; calccimimetic agents
hyperparathyroidism treatment if surgery isn’t an option?
monitor for electrolyte imbalances (Chvostek’s and Trousseau’s)
considerations following parathyroidectomy?
pseudohypoparathyroidism
genetic defect; PTH resistance at cellular level
iatrogenic hypoparathyroidism
accidental removal of parathyroid gland or vascular damage during thyroid surgery, severe hypomagnesium, tumors, heavy mental poisoning
calcium replacement therapy - give IV calcium slowly
hypoparathyroidism treatment includes -
catabolic
what reactions occur without insulin?
ketones
as the body breaks down glycogen and protein these a produced and appear in the blood and urine.
dehydration, tachycardia, orthostatic hypotension, weakness/lethargy, N/V, SOB
s/s of DKA -
Kussmaul respirations (fast, deep breathing)
breathing pattern associated with DKA -
250 ml/dl
blood sugar indicative of DKA
less than 7.2
arterial pH associated with DKA
less than 16 mEq/L
serum bicarbonate associated with DKA
K+
what electrolytes increase during DKA?
Na+, Cl-, and phosphorus
what electrolytes decrease in DKA?
replace fluids (NS .9% or .45%)
what is a priority intervention for DKA?
fluid overload, cerebral edema/increase ICP, low K+
what are you monitoring for during DKA treatment?
it will cause cerebral edema and increased ICP
why do we not want to drop blood glucose to fast?
arrhythmias (potassium drops)
what are you looking for was DKA is resolved?
no ketosis and no acidosis
what are the defining factors of HHNS?
hyperosmolar hyperglycemia nonketoic syndrome
extreme hyperglycemia and hyperosmolarity; found in type II diabetics over 60 years old
enough insulin is made to prevent DKA
why do type two diabetes go into HHNS rather than DKA?
over 600 mg/dL
what is a normal blood glucose for HHNS
elevated BUN and creatinine, glycosuria
what are labs associated with HHNS
IV insulin and NaCl infusion and rapid fluid replacement
priority treatment of HHNS includes -
correct underlying cause
what is the main goal of treatment for HHNS?
acromegaly
too much growth hormone; most often a GH-secreting pituitary adenoma
increase in triglycerides
what lab values are indicative of acromegaly?
anterior pituitary
what gland is involved in acromegaly?
7-9 years
how long does it take to diagnosis acromegaly?
sleep apnea (narrow airway), muscle weakness, neuropathy, muscle weakness
more serious manifestations of acromegaly -
DM, HTN, angina, CHF, atherosclerosis
a person with acromegaly is likely to develop -
oral glucose test
definitive test for acromegaly -
normal - GH levels will drop as glucose increases
acromegaly - GH will remain elevated as glucose increases
what is a normal response to a oral glucose challenge? what would indicate acromegaly?
CV, sleep apnea, diabetic complications
what issues will persist in a patient with acromegaly following treatment?
somatostatin analogs
preferred treatment of acromegaly; regulates and inhibits release of GH
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