complex #2 - endocrine

corticotrophin-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