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OPT Endocrine

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