Thyroid goiter Flashcards
1
Q
Goiter
A
- 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
2
Q
Normal thyroid size/requirements and endemic goiter
A
- 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)
3
Q
Pathophysiology of goiters
A
- 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)
4
Q
Types of goiters on PE
A
- 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)
5
Q
Toxic multinodular goiter
A
- 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
6
Q
Rx for multinodular toxic goiter
A
- 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
7
Q
Iodine-induced thyrotoxicosis
A
- 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
