Thyroid goiter

Question 1

Goiter

Answer 1

• Enlarged thyroid gland
• A diffuse goiter is usually due to an intrinsic inefficiency in the production of thyroid hormone
• This is secondary to a lack of iodine, adefect in the ability to utilize iodine or in the TPO nz system
• Things to ask: etiology of goiter, thyroid status, H/P (Sx of hyperthyroidism, size/consistency/mobility of the gland), TSH level/antiTPO titer

Question 2

Normal thyroid size/requirements and endemic goiter

Answer 2

• Thyroid gland requires 150-200ug iodine daily and normal gland weight 15-20g
• Reduced iodine intake results in endemic goiter: there is growth of the gland to in an attempt to compensate for inadequate hormone production
• Endemic goiter: pts are usually euthyroid, however if severe the pts may have compensated hypothyroidism (high TSH and low T4
• Doesn’t occur in US, but does in other parts of the world (mexico)

Question 3

Pathophysiology of goiters

Answer 3

• There can be a defect in TPO function
• Partial inability to iodinate Tg leads to euthyroidism + goiter
• Complete inability to iodinate Tg leads to hypothyroidism + goiter
• Poorly iodinated Tg promotes compensatory growth of gland to maintain euthyroid status
• Due to local IGF1 production and action on the gland, plus action of TSH
• There is preferential production of T3 in an effort to conserve iodine (T4 levels fall)

Question 4

Types of goiters on PE

Answer 4

• Endemic goiters are firm and may be smooth or nodular
• Grave’s disease goiters are diffusely enlarged, smooth, and squishy
• Hashimoto’s disease goiters are diffusely irregular and rubbery (like a LN)
• IMPORTANT: R side of thyroid is usually larger than left, this is consistent w/ goiter (if L side is larger think neoplasia/nodule)

Question 5

Toxic multinodular goiter

Answer 5

• Is a possible outcome of any longstanding goiter (usually occurs in 40s)
• Produces hyperthyroidism, due to proliferation of autonomous follicular cells-> multiple autonomously functioning nodules
• Could be from retained fetal follicular cells w/in adult thyroid
• Or from activating TSH receptor (constitutively active) mutations lead to autonomous T4/T3 producing clones
• May be related to an increase in iodine uptake (acute: 6-8 wks or chronic: 2 yrs)
• Labs: elevated T3/T4 (T3:T4 <18:1), low TSH, antiTPO negative, normal RAUI w/ patchy pattern

Question 6

Rx for multinodular toxic goiter

Answer 6

• Acute: use tapazole and BBs if indicated by Sxs
• Chronic: render euthyroid, preferably by total thyroidectomy
• Can use I131 if not a surgical candidate
• Repeat TSH/FT4 levels 6-8 wks post surgery (remember TSH will lag and probably still be low)
• Place on LT4 once hypothyroid to return to euthyroid

Question 7

Iodine-induced thyrotoxicosis

Answer 7

• Jod basedow disease, due to increased iodine intake when large goiter is present
• During iodine deficiency there is increased machinery to make thyroid hormone, but no iodine
• Once iodine is supplied there is excessive T4/T3 production leading to hyperthyroidism
• Usually occurs years after moving from iodine-deficient to iodine-replete environment
• Therefore increased dietary iodine intake must be done slowly to avoid this
• IMPORTANT: drugs (IV contrast) can produce hyperthyroidism when administered to pts w/ goiter