Sign and Symptoms
Amenorrhea
Decreasesed libido
Gynecomastia
proximal muscle weakness and hyperreflexia
Onycholysis
Palpitation
Osteopenia
Hypercalcemia
Hyperdefication
Non Hyperthyroid thyrotoxicosis etiologies
**Ingestio of hormone:
*pharmacologic
LT4
Liothyronine (Cytome)
Armour (mix)
* non pharmacologic
Dietary supplements
Meat products in the past
**Inflammation causing release of endogenous thyroid hormone
Hyperthyroid etiologies
*Antibody mediated
** Graves Disease
*Atuonomously functioning orthotopic thyroid tissue
** Toxic MNG
** Toxic adenoma
**Iodine exposure
* Autonomously functioning heterotopic thyroid tissue
**Struma ovarii
**Metastatic thyroid cancer
Most common
88%
10%
1 %
< 1%
Grave’s Disease
Atuoimmune Thyroid stimulating immunoglobulins
Complication
Graves ophthalmopathy
Dermopathy (pretibial myxedema)
Toxic Adenoma
Plummer’s disease
Single autonomously functioning
Nodule is usually larg
Tx: resection, antithyroid, RAI
Toxic MNG
Multiple autonomously functioning hyperplastic thyroid nodule
May be due to precipitated by I exposure
More common in elderly
Tx: RAI, surgical resection, antithyroid meds
Sensitive index of thyroid function :
TSH vs FT4 vs FT3
TSH
Radioactive tracers how are they different
I 123
Tc 99
Uptake study
Thyroid Scan
Used to generate images that reflect distributio of activity
I123 or Tc99 used / Gamma camera used to aquire images
works with looking at the distribution of the gamma radiation.
Low uptake < 2%
if low - injextion of exogenous thyroid
if high - inflammitory picture
Hyperthyroid treatment:
Antithyroid Drug
30-60% remission rate within 12-18 montsh
PTU T4-T3 inhibition
Random facts
Which is used most?
which one is good for pregnancy (1st trimaster)?
MMi most commonly used
PTU 1st trimaster / hyperthyroidism with high FT3
RAI and Pregnancy
Avoid pregnancy and breast feeding
avoid prenancy for 6 post treatment
GRAVEs and RAI
Eye Dz may exacerbate
transient increase thyrotoxicosis
Wolff–Chaikoff effect
Autoregulatory phenomenon that inhibits organification in the thyroid gland, the formation of thyroid hormones inside the thyroid follicle, and the release of thyroid hormones into the bloodstream.
This becomes evident secondary to elevated levels of circulating iodide. Lasts several days (around 10 days), after which it is followed by an “escape phenomenon”,[7] which is described by resumption of normal organification of iodine and normal thyroid peroxidase function. “Escape phenomenon” is believed to occur because of decreased inorganic iodine concentration secondary to down-regulation of sodium-iodide symporter (NIS) on the basolateral membrane of the thyroid follicular cell.
RAI of toxic adenoma and toxic MNG