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- Hypothyroidism of pregnancy
- Thyroiditis I 123 uptake usually decreased Hashimoto’s thyroiditis
- Subacute granulomatous
- Treatment
- Thyroid Neoplasms (thyroid nodules) Common, occur in 5% of adults Presentation
- Complications of surgery
- Reasons
- Parathyroid carcinoma rare / invasive / squamous / mets to lung, head/neck, kidney, ovary As part of multiple endocrine neoplasia
- Complications
Subclinical HypothyroidismLabs: elevated serum TSH and normal T4 or free T4 concentration (and no symptoms) Treatment: individualized / replacement recommended with TSH > 10 or > 5 with goiter or thyroid antibodies / otherwise, can just wait and see Course: does not always lead to primary hypothyroidism / women with increased TSH and thyroid Ab’s have 5% annual incidence of overt hypothyroidism / those pts over 65 yrs with both findings usu. develop hypothyroidism within 4 yrs / euthyroidism with reset thyrostat may not progress to hypothyroidism (probably from subtle insult to thyroid gland) Hypothyroidism of pregnancy 1-2% incidence of hypothyroidism in young women / hypothyroidism causes impaired cognitive development and increased pregnancy causes increase in levothyroxine requirement by 5th week gestation / recommendation is increase replacement dose by 30% at start of pregnancy and adjust based on TFT’s thereafter Thyroiditis I123 uptake usually decreased Hashimoto’s thyroiditis autoimmune disease / most common cause of hypothyroid in US / may have non-tender goiter (rubbery with scalloped borders) / can check for anti-microsomal Ab’s (also called anti-thyroperoxidase or TPO) / Pathology: Hurthle cells Subacute granulomatous thyroiditis (DeQuervrain’s) Presentation: pain, tenderness, symptoms of hyperthyroid (usu. takes about 6-8 weeks to achieve spontaneous remission) / often associated with viral illness (URI, etc.) Diagnosis: clinical and/or I123 scan Findings: increased free T4 or FTI but decreased I-123 uptake because of the follicular cells’ inability to concentrate iodine Treatment: treat symptoms (NSAIDs, B-blockers, may need steroids) / PTU/M not effective Subacute lymphocytic thyroiditis common post-partum / unknown etiology / painless Riedel’s thyroiditis (Struma) unknown etiology / can compress neck structures and/or cause hypothyroidism / fibrosis of gland / PET-scan may be useful in diagnosis Medications: amiodarone-induce (side effect), iodine or T4 (factitious or overdose) Other causes: TSH-secreting pituitary adenoma, hydatidiform moles, choriocarcinomas (hCG secretion), ovarian teratomas, metastatic follicular thyroid carcinomas Thyroid Neoplasms (thyroid nodules) Common, occur in 5% of adults Presentation: nodules usually painless unless they ulcerate or compress other things Diagnosis: if incidentally discovered by imaging, small (< 1 cm), normal TSH, asymptomatic, no h/o radiation or thyroid cancer, can watch and re-evaluate in 6 months, otherwise… I-123 radioactive uptake scan (cold has 5-10% chance of malignancy probably need to do FNA (15% will be suspicious and require surgical evaluation) / ultrasound shows cystic or solid (but still probably will need FNA or Bx) / pentagastrin test for medullary carcinoma Ddx: follicular adenoma, multinodular goiter, colloid nodule, Hashimoto’s, cyst, lymphoma, mets, parathyroid 90% of all thyroid nodules benign (incidental, < 1 cm even more likely benign) nodules increase with age (younger patient means increased chance of malignancy) nodules usually cold (do not take iodine) Treatment: Iodide may be used to decrease vascularity (pre-op for thyroid resection) / excision +/- lymph node dissection / if thyroid completely removed, then lifelong exogenous T4 to suppress TSH production (keep TSH at barely detectable levels) / follow-up I-123 uptake scan to ensure no active thyroid tissue present Complications of surgery: 50% becoming hypothyroid (complications: recurrent and superior laryngeal nerve paralysis, recurrence and hypoparathyroid), may have to remove hyoid to remove all accessory tissue Follicular adenoma encapsulated / usually euthyroid / Treatment: as above Thyroid Carcinomas Papillary carcinoma - good prognosis 1st in U.S. / indolent (slow growth), +/- bilateral Pathology: ground-glass nuclei, longitudinal nuclei, psammoma bodies lymphatic spread / previous irradiation gives a 2-fold higher risk Exam: may have lymphadenopathy (mets), even with normal thyroid palpation Follicular carcinoma - bad prognosis 2nd in U.S. / vascular spread (brain, bone, etc) / middle aged women / may mimic follicular adenoma Medullary carcinoma - bad prognosis 3rd in U.S. / lymphatic spread / bilateral / parafollicular C-cells / secrete calcitonin / FH of disease is better / isolated or as part of MEN II and III Undifferentiated (anaplastic) - extremely bad prognosis radiation + chemotherapy is only palliative Parathyroid Physiology Total serum calcium 9 mg/dl – bound to proteins (albumin) and PO4 / regulated indirectly Ionized serum calcium 4.5 mg/dl – regulated directly PTH increases bone resorption (osteoclast activation) increases serum calcium lowers fractional reabsorption of PO4 from kidney (normally set at 80-90%) increases formation of 1,25-OH – increases Ca and PO4 absorption in GI increases urinary cAMP Vitamin D causes GI absorption of PO4, Ca and increased renal PO4 and Ca reabsorption, and lowers PTH Vitamin D deficiency occurs in 25% of elderly / affects seen in children more acutely due to lower calcium stores in bones/ may cause lowered Ca and PO4 leading to secondary hyper PTH Reasons: lower intake, lack of sun exposure, direct renal damage (conversion enzymes), anticonvulsants (increased inactivation) Labs: 25-OH – 1000 fold higher than 1,25-OH – useful to measure vitamin D deficiency 1,25-OH – useful for diagnosis hypercalcemia caused by secretory tumor Treatment: 1000-2000 vitamin D / 1 to 1.5 g Ca supplement Calcitonin increases renal excretion of calcium / increases bone formation [more like an escape mechanism / not a primary regulator of serum calcium] PTHrP protein functions identically to PTH causing hypercalcemia / can be measured directly by lab Hyperparathyroidism (other causes of hypercalcemia) Not uncommon (3 in 1000 middle-age women) / female 2x > male (usually after puberty) Causes: primary adenoma (90%), secondary adenoma, carcinoma, MEN I (10%) Increased PTH: pancreatitis, nephrolithiasis, nephrocalcinosis, gout, pseudogout, HTN, PUD Presentation: can present in hypercalcemic crisis Bones: renal stones, UTI, renal failure, nephrocalcinosis (less common) Stones: aches, arthralgias, pseudogout Abdominal groans: dehydration, constipation, pancreatitis, PUD (CA stimulates gastrin secretion), nausea, vomiting Psychic overtones: anorexia, personality changes, polyuria/polydipsia Fatigue: muscle fatigue or atrophy, lassitude Labs: Hypercalcemia Hypercalciuria only seen in 2/3 of cases Alk phos only ↑ with significant bone disease serum chloride ↑ due to PTH-induced bicarbonaturia (more consistent finding than hypophosphatemia) Parathyroid hyperplasia chief cell - solid area of chief cells, reduced fat clear cell - uniform distribution of clear cells, reduced fat
multiple myeloma, Paget’s, Addisonian crisis, familial HH? Treatment: resection for hyperplasia (leave ½ of 1 gland) / adenoma (remove only 1 gland) / can cause ‘hungry bones’ phenomenon (hypocalcemia) – perioral numbness, Chvostek’s, seizures / 5% recur (can re-operate) Parathyroid carcinoma rare / invasive / squamous / mets to lung, head/neck, kidney, ovary As part of multiple endocrine neoplasia (see other) Secondary hyperparathyroidism (renal osteodystrophy) CRF ↑ serum PO4 CaPO4 deposition ↓ serum Ca ↑ PTH release ↓ vitamin D-1-25-OH (due to renal failure) ↓ serum Ca ↑ PTH release Complications: osteodystrophy, myopathy, can get severe muscle atrophy Treatment: vitamin D supplementation, ↓ PO4 intake, PO4 binders (calcium carbonate) Download 3.95 Mb. Share with your friends:
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