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OPT Endocrine

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Term
Definition
feedback inhibition   increased activity of target tissue down regulates secreting gland  
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pituitary gland   bean-shaped gland at base of brain, connected to hypothalamus  
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adenohypophysis   anterior lobe of the pituitary; secretes FSH, LH, ACTH, TSH, PRL, GH  
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neurohypophysis   posterior lobe of the pituitary; secretes {ADH} and {oxytocin}  
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1. visual field abnormalities 2. elevated intracranial pressure   symptoms of pituitary mass effects:  
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prolactinoma   most common type of hyper functioning pituitary adenoma; amenorrhea, lactation, infertility  
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growth hormone-producing adenomas   excess GH causes {gigantism} before epiphyses close and {acromegaly} if after closure; neoplasms of somatotrophs  
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Cushing syndrome   neoplasm of corticotroph cells that make ACTH causes hypercortisolism  
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gonadotroph adenoma   neoplasm of excess LH or FSH  
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thyrotroph adenomas   neoplasm of excess TSH  
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hypopituitarism   usually acquired diseases intrinsic to the pituitary  
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nonfunctioning pituitary adenomas   neoplasms that mostly exhibit mass effects  
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ischemic necrosis of the anterior pituitary   most commonly seen in {Sheehan syndrome} after pregnancy  
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ablation of pituitary by surgery or radiation   pituitary hypo function from inflammatory conditions  
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pituitary dwarfism   ablation of pituitary gland can cause a GH deficiency in children and they fail to grow  
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posterior pituitary syndromes   clinically important syndromes that involve ADH that is usually released when decreased water concentration in plasma  
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diabetes insipidus   ADH deficiency causes excessive urination because kidney does not resorb water; polydipsia and polyuria  
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central diabetes insipidus   type of diabetes insipidus from ADH deficiency  
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nephrogenic diabetes insipidus   type of diabetes insipidus from renal tubular unresponsiveness but normal ADH levels  
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syndrome of inappropriate ADH secretion (SIADH)   excess ADH production so resorption of excessive water; most commonly from ectopic ADH secretion from tumors and head trauma  
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thyroid   net result of hormones is to increase basal metabolic rate -disorders can be excess (hyperthyroidism), deficiency (hypothyroidism) and mass lesions  
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hyperthyroidism   most common cause of thyrotoxicosis; hyper metabolic state from elevated T3 and T4  
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thyroid storm   abrupt onset of hyperthyroidism; medical emergency  
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primary hyperthyroidism   decreased levels of TSH but increased T3 and T4 levels  
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Graves disease   most common cause of endogenous hyperthyroidism; an autoimmune disorder  
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1. thyrotoxicosis 2. ophthalmopathy 3. dermopathy   triad of Grave's disease  
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exophthalmos   abnormal protrusion of the eyeballs  
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pretibial myxedema   scaly thickening and orange peel texture seen in Grave's disease, especially on shins  
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hypothyroidism   deficient production of thyroid hormones  
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cretinism   hypothyroidism in childhood from lack of iodine; kids have skeletal and CNS issues  
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myxedema   hypothyroidism in older children and adults; apathy, mental sluggishness, obesity  
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primary hypothyroidism   serum TSH increased because of loss of feedback inhibition from thyroid  
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chronic lymphocytic (Hashimoto) thyroiditis   most common cause of hypothyroid disease in areas of the world where iodine is in sufficient quantities -autoimmune destruction of thyroid cells and replacement by lymphocytic cells  
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1. cytokine-mediated cell death 2. CD8 cytotoxic T-cell mediated cell death 3. antithyroid antibodies   thyrocyte death in Hashimoto's by:  
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hashitoxicosis   hypothyroidism preceded by transient thyrotoxicosis from disruption of thyroid follicles  
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diffuse and multinodular goiter   enlargement of thyroid from impaired synthesis of thyroid hormones from lack of iodine  
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superior vena cava syndrome   goiter that compresses vessels in neck and upper thorax  
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1. activation of proto-oncogene RET by chromosomal rearrangement 2. germline mutations   unique to thyroid cancers:  
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papillary carcinoma   most common type of thyroid neoplasm from radiation exposure; chromosomal rearrangement of {RET proto-oncogene} resulting in {RET/PTC fusion protein} -{NTRK1 and BRAF mutations activate MAP kinase pathway}  
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follicular carcinoma   thyroid neoplasm from iodine deficiency  
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medullary carcinoma   most cases are sporadic but some found in MEN 2A and B; caused by {germline RET mutations  
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anaplastic carcinoma   one of the most aggressive human cancers; in older patients with history of goiter  
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parathyroid glands   4 glands at corners of thyroid; composed of {chief cells} and {oxyphil cells} that secrete parathyroid hormone  
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parathyroid hormone   hormone that is controlled by free calcium levels in the bloodstream, not the pituitary  
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1. increase osteoclast activity 2. convert Vit. D to active form 3. increase Ca reabsorption in kidneys   3 ways PTH increases calcium levels  
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hyperparathyroidism   on radiograph, bone looks like {ground (frosted) glass} and is osteoporotic  
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osteitis fibrosa cystica   replacement of resorbed bone by fibrous tissue with cysts; from hyperparathyroidism  
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brown tumors of hyperparathyroidism   aggregates of osteoclasts, giant cells and hemorrhagic debris  
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metastatic calcification   can be secondary to hypercalcemia  
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primary hyperparathyroidism   one of the most common endocrine disorders; causes {hypercalcemia} and often brought on by a parathyroid adenoma -painful bones, renal stones, abdominal groans and psychic moans  
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secondary hyperparathyroidism   chronic calcium depression, usually from {renal failure}  
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renal osteodystrophy   bone abnormalities seen in patients with renal failure and hyperparathyroidism  
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tertiary hyperparathyroidism   parathyroid activity becomes autonomous and excessive  
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hypoparathyroidism   much less common than hyperparathyroidism; hypocalcemia, muscle spasms, dental abnormalities  
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DiGeorge syndrome   congenitally missing parathyroid glands that causes symptoms of hypoparathyroidism  
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adrenal gland   paired organs with cortex and medulla; makes glucocorticoids, mineralocorticoids and sex steroids  
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adrenal medulla   contains chromaffin cells that make catecholamines, mainly epinephrine  
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1. hypercortisolism (Cushing syndrome) 2. hyperaldosteronism 3. adrenogenital syndromes   3 clinical syndromes of adrenocortical hyperfunction (hyperadrenalism)  
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Cushing syndrome (hypercortisolism)   any elevation of glucocorticoids; buffalo hump, moon faces, truncal obesity, hypertension and weight gain  
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primary adrenocortical hyperplasia or neoplasm   autonomous adrenal function independent of the levels of ACTH  
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primary hypothalamic-pituitary disease aka Cushing disease   over-secretion of ACTH with increased skin pigmentation  
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secretion of ectopic ACTH by non-pituitary neoplasms   small-cell lung carcinomas can have this effect  
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hyperaldosteronism   excess aldosterone causes sodium retention and potassium excretion--leads to hypertension and hypokalemia  
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secondary hyperaldosteronism   accompanied by increased levels or renin  
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primary hyperaldosteronism / Conn's syndrome   caused by an aldosterone-producing neoplasm with low renin levels  
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congenital adrenal hyperplasia (CAH)   recessive defect in an enzyme for adrenal steroid biosynthesis with an increase in ACTH; type of adrenogenital syndrome  
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21-hydroxylase deficiency   most common enzymatic defect in CAH; required for cortisol and aldosterone  
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adrenal insufficiency   only apparent if 90% compromised; can be acute, chronic, or secondary insufficiency  
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Waterhouse-Friderichsen syndrome   massive adrenal hemorrhage secondary to sepsis that can cause acute adrenal insufficiency  
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chronic adrenocortical insufficiency (Addison Disease)   progressive destruction of adrenal cortex with increase in ACTH and pigmentation  
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1. autoimmune adrenalitis 2. tuberculosis 3. acquired immune deficiency syndrome (AIDS) 4. metastatic cancers   causes of chronic adrenocortical insufficiency  
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secondary adrenocortical insufficiency   any disorder that reduces ACTH production; aldosterone levels and pigmentation remain normal  
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adrenal adenomas   benign adrenal tumors with little consequence  
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adrenocortical carcinoma   rare adrenal tumors that are very metastatic (most tumors in adrenal cortex are not primary tumors)  
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pheochromocytoma   neoplasms of chromaffin cells that release catecholamines, hypertension; uses rule of 10's (10% outside adrenal gland, 10% bilateral, 10% malignant)  
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multiple endocrine neoplasia syndromes   group of dominantly inherited diseases resulting in proliferative lesions of endocrine glands  
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MEN 2   both Type 2A and 2B have gain-of-function mutations of RET proto-oncogene  
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multiple endocrine neoplasia 2A   involve the thyroid (medullary carcinoma of the thyroid), adrenal medulla (adrenal pheochromocytomas) and parathyroid gland  
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multiple endocrine neoplasia 2B   distinct germline mutation of one amino acid; like MEN 2A but no parathyroid symptoms -also get {mucosal neuromas} and {ganglioneuromas}  
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