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Hypothalamic-Pituitary-Thyroid Axis
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Hypothalamic-Pituitary-Thyroid Axis
- -Thyroid secretes thyroxine (T4) and Triiodothyronine (T3)
- -T4 (85%), T3 (15%)
- -T3 is the active hormone and binds nuclear receptors
- -most T3 comes from peripheral deiodination of T4
- -T4/T3 are mostly bound to TBG
- -T3 negatively regulates TSH
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Thyroid Hormone Synthesis
- -Iodine enters thyrocyte by NIS transporter
- -TPO organifies Thyroglobulin and iodine --> Tg bound to T3 and T4
- -thyroglobulin is stored in colloid
- -TSH binding triggers endocytosis of Tg and lysosomal proteolysis to release T3 and T4
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Euthyroid
Normal TSH (bellcurve shape: 0.3 to 4, median 1.5)
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Log-Linear Relationship bwtn T4 and TSH
- -small change in T4 causes a large change in TSH
- -can pick up mild thyroid dysfunction with TSH
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Causes of Alterations in TBG
- 1. Elevated TBG
- -estrogens (OCPs, pregnancy)
- -acute hepatitis
- 2. Decreased TBG
- -androgens
- -glucocorticoids
- -liver failure
- -nephrotic syndrome
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Hypothyroidism: Symptoms
- Cold Intolerance (decreased heat production)
- Weight Gain (decreased appetite)
- Hypoactivity, lethargy, weakness
- Constipation
- Decreased reflexes
- Myxedemal (facial/periorbital)
- Dry cool skin
- Brittle Hair
- Bradycardia
- Dyspnea on exertion
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Hypothyroidism: Myxedema Coma
-if hypothyroidism is severe and untreated then combined with an exacerbating medical condition symptoms can become serious
-exacerbation: trauma, infection, cold exposure, opiates
-clinical features: hypothermia, hyponatremia, bradycardia, hypotension, hypoglycemia
-50% mortality
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Primary Hypothyroidism: Causes
- 1. Iodine deficiency (most common worldwide)
- 2. Congenital thyroid disorder
- 3. Thyroid tissue destruction
- -Hashimoto's (autoimmune)
- -Radiation
- -Thyroidectomy
- -Infiltrative diseases (very rare)
- 4. Drugs
- -Li (bipolar)
- -Amiodorone (Iodine containing)
- -IFNa
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Hypothyroidism: Iodine Deficiency
- -most common cause in developing countries
- -fetal iodine deficiency (cretinism)
- -goiter (fetal hyperplasia)
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Hypothyroidism: Hashimoto's
- -autoantibodies against TPO, Tg and TSHR (blocking)
- -activated T cells cause thyrocyte apoptosis
- -can be goiterous or atrophic
- -more common in women (5:1)
- -precipitated by: infection, stress, sex steroids, pregnancy
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Post-Partum Thyroiditis
- -occurance of hyper or hypo thyroidism during the post partum period
- -autoimmune (TPOab or TSI)
- -10% have permanent hypothyroidism
- -high risk: patients with hx of autoimmune disorder
- Clinical Course:
- 1. thymocytes are damaged (ie: due to infection) --> uncontrolled release of thyroid hormones
- 2. spike in T3/T4 inhibits TSH and Iodine uptake
- 3. over 6 wks hormones are degraded until there are low serum levels --> increased TSH
- 4. no hormone stores in thyroid to release, needs time to recover

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Thyrotoxicosis
- -increased thyroid hormone in the circulation
- -most common cause: hyperthyroidism
- -determine cause by RAIU
- HIGH RAIU (hyperthyroidism)
- -autoimmine (Grave's)
- -toxic multinodular goiter
- -Toxic adenoma
- -hCG induced (choriocarcinoma, molar pregnancy)
- -TSH-secreting pituitary adenoma (rare)
- LOW RAIU (exogenous thyroid hormone)
- -iodine induced (increased hormone release)
- -thyroiditis
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Thyrotoxicosis: Symptoms
- -cardiac (tachy)
- -tremor
- -sweating
- -muscle wasting
- -prox muscle weakness
- -anxiety
- -goiter
- -increased appetite with wt loss
- -amenorrhea/oligomenorrhea
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Grave's Disease
- -TSH R stimulating antibodies (TSI)
- -more common in women (9:1)
- -age 20-40
- Symptoms:
- -diffuse goiter with homogenous RAIU
- -exopthalmos (ab against orbital fibroblasts)
- -dermopathy (ab against skin)
- -thyroid acropachy (ab against bone)
- -pretibial myxedema
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Toxic Multinodular Goiter (Plummer's Disease)
- -focal patches of hyperfunctioning follicular cells
- -independent of TSH
- -activating mutation in TSHR
- -rarely malignant
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Toxic Thyroid Adenoma
-can be treated with RAI (b/c rest of thyroid isn't taking up iodine so shouldn't be affected)
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Iodine Induced Thyrotoxicosis: Iodine sources
- 1. Diet (seaweed, kelp)
- 2. Contrast
- 3. Iodine solutions
- 4. topical antiseptics
- 5. Meds (amiodorone, expectorants)
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Hyperthyroidism: Treatment
- 1. Antithyroid drugs (methimazole, PTU)
- 2. Radioactive iodine
- 3. thyroidectomy
- 4. beta blockers
- 5. corticosteroids
- 6. Lithium
- 7. Potassium iodide
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Methimazole and PTU
- -inhibit iodination (inhibit TPO)
- -PTU inhibits 5' deiodinase (inibits peripheral T4 to T3)
- -PTU is safe in first trimester by causes hepatotoxicity
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Radioactive Iodine Treatment
- -used to tx toxic nodules or Grave's (autoabs still present but target is gone)
- -effective but slow response
- -80% develop hypothyroidism
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Lithium
- -reduces iodine binding and hormone release
- -many toxic side effects
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Potassium Iodide
- -blocks release of thyroid hormone (wolff chekoff effect)
- -used to get severe hyperthyroidism controlled quickly
- -loses effect quickly
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Thyroid Nodules: Incidence
- -common (clinically apparent in 4-7%)
- -up to 50% are incidentally discovered
- ->90% benign
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Thyroid Nodules: Workup
- 1. Check TSH (if low --> RAIU)
- 2. RAIU
- -hot nodules rarely malignant
- -5-15% of cold nodules are malignant
- 3. FNA bx (cold nodules, >1cm)
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Papillary Thyroid Cancer
- -ground glass nuclei with grooves
- -orphan annie eyes
- -good prognosis
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