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24 Cards in this Set
- Front
- Back
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Graves dz
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hyperthyroidism, autoimmune thyroid dz
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GD pathogenesis
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autoAb to TSH R on thyroid follicular cells
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GD clinical effects
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thyroid enlargement (big, smooth, soft, red, meaty), ophthalmopathy (proptosis: bulging out of eye orbit), dermopathy (pretibial myxedema: thickening of skin and not soft, thyroid acropachy: new bone formation-->clubbing)
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GD risk factors
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HLA DR3, polymorphisms in CTLA-4
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GD concordance rate
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low, 25%
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GD Dx
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thyroid hormones: TSH and free T3
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GD prognosis
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high levels of TSH-R Ab: persistent hyperthyroidism, high levels of TSH-R Ab at end of cycle of anti-thyroid Rx: relapse after Rx withdrawal
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GD and pregnancy
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forecasting of neonatal hyperthyroidism very important
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6 classic endocrine glads
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hypophysis (pituitary), thyroid, parathyroid, adrenals, pancreatic islets, gonads
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Anterior pituitary hormones
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ACTH, TSH, LH, FSH, GH, PRL (FLAT PiG)
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Posterior pituitary hormones
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T4, T3, calcitonin
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parathyroid hormones
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PTH
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Adrenal cortex
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aldosterone, cortisol, DHEA
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Adrenal medulla
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Epi, NE
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Pancreatic islets
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insulin, glucagone, somatostatin
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Testes
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testosterone, inhibin
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Ovaries
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estrogens
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Hashimoto thyroiditis forms
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classic, atrophic (primary myxedema), post-partum thyroiditis, silent (painless), focal
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Classic Hashimoto thyroiditis
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middle aged woman, goiter (eu- or hypo-), chronic course-->hypothyroid
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Classic Hashimoto thyroiditis Tx
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synthetic T4
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Dx tests
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m. TPOAb, TB Ab
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Addison dz
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adrenocortical insufficiency, decreased glucocorticoids, mineralcorticoids, androgens, and 2ndary elevation in ACTH, adrenal cortex infiltrated w/ Ly, eventually atrophic, can be in isolation or part of autoimmune polyglandualr syndrome type I or II
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Cause of Addison dz
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autoimmunity (80%), TB
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Addison dz predisposition
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MHC Class II: DR3, MHC class I-related molecule A, Ab to 21-hydroxylase
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