Thyroid dz Meds Flashcards
etiologies of primary hypothyroidism? etiology of iatrogenic hypothyroidism?
primary: autoimmune phenomena (Hashimoto’s dz), malnutrition, deficient iodine intake
iatrogenic: surgery or radioactive ablation
what does secondary hypothyroidism imply? tertiary?
secondary implies pituitary dysfunction
tertiary implies hypothalamic dysfunction
what can inflammation of the thyroid gland result in? thyroiditis course?
in initial excess thyroid release which is then followed by a period of insufficient thyroid hormone release
course of thyroiditis is usu limited and reversible except in Hashimoto’s
clinical findings of hypothyroidism?
fatigue, weakness, cold intolerance, constipation, thinning hair, bradycardia, poor concentration
if chronic can result in respiratory depression, hypothermia, coma (myxedema coma), death
infants w/unrecognized and untreated hypothyroidism develop cretinism
3 hypothyroid tx options?
levothyroxine (T4)/synthroid
thyroid USP (T4, T3)/Armour thyroid
Liothyronin (T3)/Cytomel
class of levothyroxine/synthroid? indications? MOA?
class: thyroid hormone replacement, synthetic T4, dosed in mcg
indications: hypothyroidism, also TSH suppression in select cases of thyroid nodules and thyroid CA
MOA: replaces normal levels of T4 and T3 (T4 converted to T3 in periphery)
how to give levothyroxine/synthroid? how long to tx? when to hold or reduce dose?
give PO/IV once a day
oral absorption ~70%
slow onset of action
1/2 life 1 wk
takes 6-8 wks to achieve steady state
tx usu lifelong - need to follow pts clinical response and serum TSH
hold or reduce dose if any complaints of angina
begin at low dose and advance dosage slowly in pts over 65 or in any pts w/hx of coronary artery dz
SEs of levothyroxine/synthroid? long term elevation of T4 can cause what?
SEs: toxicity directly related to thyroxine level and manifests as palpitations, tachycardia, intolerance to heat and anxiety
long term elevation of serum T4 may accelerate cardiac dz and osteoporosis
in pts w/Addison’s dz and hypothyroidism what needs to be replaced first?
need to give cortisol first! then thyroid otherwise can be fatal
60 mg of Thyroid USP produces about an equivalent effect of how much synthroid?
60 mg of Thyroid USP = about 100 mcg of Synthroid (synthetic T4)
class of thyroid USP/armour? indications? mOA? how to give? how to dose?
class: thyroid hormone (T4, T3, T2, T1) from desiccated animal thyroid gland
indications: hypothyroidism
MOA: replaces both T4 and T3
give PO, generally standardized to iodine content
initiate medication at low dose and increase dosage according to pt response, more cautious dosing in pts over 65 or if hx of cardiac dz
SEs of thyroid USP/Armour? what do you need to follow? hold or reduce if complaints of what? how to dose?
SEs: similar to thyroxine/synthroid
follow pts clinical response and serum TSH
hold or reduce dose if any complaints of angina
begin at low dose and advance dose slowly in pts over 65 or in those w/hx of CAD
class of liothyronine/cytomel? indications? can also be used for what? MOA?
class: thyroid hormone replacement (synthetic T3) dosed in mcg
indications: hypothyroidism that has demonstrated intolerance to T4 replacement therapy or no improvement on T4 replacement therapy, myxedema coma
also used for Wilson’s syndrome
MOA: replaces T3
how to give liothyronine/cytomel? SEs? higher peaks and troughs of T3 can increase what risk?
give PO/IV, 100% oral absorption, rapid onset of action, half life of several hours
SEs: similar to T4
higher peaks and troughs of T3 may increase risk of coronary artery disease and osteoporosis
equivalent dosings between thyroid USP, synthroid and cytomel?
60 mg thyroid USP ~ = 100 mcg of T4 (synthroid) ~ = 25 mcg of T3 (cytomel)
most common underlying cause of hyperthyroidism?
autoimmune - Grave’s - antibodies stimulate TSH receptor sites on the thyroid gland
can also be caused by thyroiditis
what is thyroiditis facticia?
excess administration of thyroid hormone, either inadvertent or intentional
clinical findings of hyperthyroidism include? hyperthyroidism places pt at increased risk for what?
nervousness, tachycardia, wt loss, heat intolerance, sweating, diarrhea, generalized weakness
places the pt at increased risk for osteoporosis and cardiac dz
if dt Grave’s dz often accompanied by presence of goiter and exophthalmos
what is pretibial myxedema? associated with what? dt what?
lesions of non-pitting edema that occur in association w/Grave’s dz
appear on anterior or lateral aspects of legs in ~0.5-5% of pts w/Grave’s dz
dt deposition of hyaluronic acid in dermis and subcutis in thyroid dz
proposed mechanism is that fibroblasts are stimulated to produce high amounts of glycosaminoglycan dt exposure to thyroid hormones
tx of hyperthyroidism involves what? what can be used to block teh adrenergic ssxs of hyperthyroidism?
tx involves medications that interrupt thyroid hormone synthesis and/or release of thyroid hormone as well as interruption of peripheral conversion of T4 to T3
beta blockers are often used to block adrenergic ssxs of hyperthyroid state
definitive tx of hyperthyroidism?
surgical removal of radioactive iodine and ablation of the thyroid gland
after this though pts are rendered hypothyroid and will need exogenous thyroid hormone for the rest of their lives
hyperthyroid tx options?
methimazole propylthiouracil propanolol iodine radioactive iodine
class of methimazole/tapazole? indications? place in tx of hyperthyroidism? after tx is discontinued what can happen? tx failure or recurrence suggests what tx is needed?
class: thioamide
indications: hyperthyroidism dt Grave’s dz, toxic nodular or toxic multinodular dz and thyroid storm (when give IV)
can allow for better control of hyperthyroid state until more definitive tx is used
pts may occasionally achieve a euthyroid state after tx is discontinued
tx failure or reucrrent of hyperthyroid state suggests more definitive tx is necessary
MOA of methimazole/tapazole? how to give? where does it concentrate? effects on thyroglobulin already stored in thyroid gland?
MOA: inhibits transformation of inorganic iodine to organic iodine, therefore blocking production of thyroxine, also inhibits coupling of iodotyrosine to form T3 and T4, very minimal effect of blocking the peripheral conversion of T4 to T3
give PO, IV (thyroid storm)
concentration occurs in thyroid
does not affect thyroglobulin already stored in thyroid gland