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EDGEWOOD COLLEGE School of Nursing N 312 Drugs for Thyroid Disorders Four steps in synthesis of thyroid horones! 1" tr#nsport #nd concentr#tion of iodide into thyroid 2" iodide undergoes o$id#tionto for iodine %en&ye pero$id#se needed' 3" #cti(#ted iodine )ecoes incorpor#ted into tyrosine residues *" iodin#ted tyrosine olecules #re coupled T4: thyroxine (half-life of 1 week) T3: triiodothyronine (half life of 1.5 days) TSH: thyroid stimulatin hormone (most sensiti!e for dianosin hy"othyroidi # Hy"erthyroidism $ hy"era%ti!ity of the thyroid land& se%retin ex amounts of thyroid hormones. 'ra!e s disease& an autoimmune disorder& is the most %ommon form. Treated with antithyroid drus& radioa%ti!e iodine or sur Sins and sym"toms- ele!ated H*& "al"ations in %hest& anxiousness& insomnia& intoleran%e to heat& in%reased a""etite& weiht lost& dee" tendon reflexes !e a%ti!e +T, %propylthiour#cil'! inhi+its at Ste" , (oxidation of iodide) and Ste ("re!ents iodinated tyrosine from %ou"lin). lso inhi+its %on!ersion of T4 in "eri"hery. T/ does not destroy existin stores of thyroid hormone& theref may take 1-, weeks to take effe%t. ntithyroid 0ral medi%ation #nhi+its %on!ersion of T3 T4 to a%ti!e form a2or side effe%t: aranulo%ytosis ( ) -l#c. )o$ /#rning 0 a%ute li!er failure 1617&777 s6s a+d. ain& 2aundi%e& 8 a""etite. #dio#cti(e odine %131 '! destroys thyroid tissue +y emission of +eta "arti%les. d!antaes: low %ost& no surery& not life-threatenin& no other tissue dest 9isad!antaes: delayed onset $ u" to se!eral months& sinifi%ant ons hy"othyroidism ( 17-37;)

N 312 Thyroid-steroids

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EDGEWOOD COLLEGE

EDGEWOOD COLLEGE

School of Nursing

N 312

Drugs for Thyroid Disorders

Four steps in synthesis of thyroid hormones:

1. transport and concentration of iodide into thyroid

2. iodide undergoes oxidation to form iodine (enzyme peroxidase needed)

3. activated iodine becomes incorporated into tyrosine residues

4. iodinated tyrosine molecules are coupled

T4: thyroxine (half-life of 1 week)

T3: triiodothyronine (half life of 1.5 days)

TSH: thyroid stimulating hormone (most sensitive for diagnosing hypothyroidism)

I Hyperthyroidism hyperactivity of the thyroid gland, secreting excessive amounts of thyroid hormones. Graves disease, an autoimmune disorder, is the most common form. Treated with antithyroid drugs, radioactive iodine or surgery.*Signs and symptoms- elevated HR, palpations in chest, anxiousness, insomnia, intolerance to heat, increased appetite, weight lost, deep tendon reflexes very activePTU (propylthiouracil): inhibits at Step 2 (oxidation of iodide) and Step 4 (prevents iodinated tyrosine from coupling). Also inhibits conversion of T4 to T3 in periphery. PTU does not destroy existing stores of thyroid hormone, therefore may take 1-2 weeks to take effect. Antithyroid

Oral medication

Inhibits conversion of T3 T4 to active form

Major side effect: agranulocytosis (( WBC)

*Black box warning acute liver failure 1/10,000 s/s abd. Pain, jaundice, appetite.

Radioactive Iodine (131 I): destroys thyroid tissue by emission of beta particles.

Advantages: low cost, no surgery, not life-threatening, no other tissue destroyed

Disadvantages: delayed onset up to several months, significant onset of hypothyroidism ( = 10-30%)

Propranolol beta-blocker used to treat S/S of hyperthyroidism until drugs take effect.

Hypothyroidism: severe form in adults> myxedema. In children> cretinism.

In iodine sufficient areas, principle cause is autoimmune thyroiditis (Hashimotos

Disease). Other causes are insufficient iodine in the diet put in salt now,

iatrogenic from tx. of hyperthyroidism.

**common disorder

**often as a result of being treated for hyperthyroidismLevothyroxine (T4) synthroid: synthetic thyroid replacement. Taken orally without

food. Often life-long therapy is needed. If excessive, danger of thyroid storm or

thyrotoxicosis developing. Has a long half-life, 7 days, takes 28 days to reach peak.Thyroid Storm:-excesive hormone release

-very elevated HR, BP

-can be treated with beta-blockersEvery day dosing necessary. Need to monitor closely in those with cardiovascular

disease.

(absorption with aluminum antacids, ferrous sulfate, calcium supplements

( effects of warfarin (coumadin)

Corticosteroid therapy in non-endocrine disorders

Corticosteroids: powerful anti-inflammatory and immunosuppressive action.

Normally, released by the adrenal glands. Made up of mineralocorticoid and

glucocorticoid hormones. Also, regulate electrolyte balance by sodium and water reabsorption. Regulate protein, carbohydrate, and fat metabolism.

Therapy for long-term management of chronic inflammatory diseases, such as

rheumatoid arthritis, lupus, colitis, asthma, & COPD. Used for suppression of

inflammatory response during organ transplant. Therapy for short-term tx. of acute dermatitis, bronchitis, spinal cord injury and soft tissue injury. Available as an oral, parenteral, topical,

inhaler, and ophthalmic ointment.

Disadvantage: steroids affect the bodys metabolic functions, they should be given

only when the benefits outweigh the risks. There are many associated side effects with

long-term corticosteroid therapy. * can reactivate TB, should not be used with a live virus administration since inflammatory response is suppressed*contraindicated

in fungal infections.

Prednisone inhibits release of mediators that promote the inflammatory response.

Inhibit release of macrophages and inhibit increase in vascular permeability. Promotes

protein, fat, carbohydrate breakdown.

Side effects: inhaled steroid use ( risk for oral candidiasis (yeast infection)

At risk for hypokalemia, monitor drug interactions that also cause loss of K+. Impaired wound healing, osteoporosis, weight gain, development of diabetes.

Long-term use will suppress the normal function of the adrenal gland. If steroids are suddenly stopped the adrenal gland is unable to secrete.

DO NOT STOP DRUG - MUST TAPER - Can be life threatening.