ࡱ> {` bjbjFF 4,,WR,VVVV8W,y|WWWWW/Z/Z/Zxxxxxxx$W{h}xZ\Y@/ZZ\Z\xWWybjbjbjZ\ RWWxbjZ\xbjbjnwh"xWW PMViLwxy0ywg~6jg~ xg~x,/ZhZJbjZ<[=/Z/Z/ZxxRj/Z/Z/ZyZ\Z\Z\Z\,,,-1$,,,1,,, ENDOCRINE DISORDERS Thyroid Disorders Hyperthyroidism Etiology: Graves Disease / Diffuse Toxic Goiter (MC): AI disorder where thyroid-stimulating IgG binds to TSH receptors on thyroid cells and triggers synthesis of excess thyroid hormone - - shown as diffuse uptake on radioiodide scan Plummers Disease / Multinodular Toxic Goiter: hyperfunctioning areas of the thyroid cause increased production of T3 and T4 thereby causing a decrease in TSH, which leads to atrophy of normal thyroid tissue - - shown as patchy uptake on scans Hashimotos thyroiditis and subacute thyroiditis ( transient postpartum thyroiditis, iodine-induced thyroiditis, (-dose Synthroid Symptoms: Nervousness, insomnia, irritability, hand tremor, hyperactivity, excessive sweating, heat intolerance, weight loss with increased appetite, frequent defecation, palpitations, muscle weakness Signs: Graves = symmetric nontender enlargement of thyroid; bruit Subacute thyroiditis = exquisitely tender, enlarged; precedent viral URI Plummers/Hashimotos = bumpy, irregular, asymmetric Toxic Adenoma = single nodule, atrophic Proptosis (edema of EOM and retro-orbital tissue) in Graves disease, arrhythmias, HTN, warm moist skin, pretibial myxedema (accumulation of mucopolysaccharides), hyperactive DTRs, tremor Dx: Low serum TSH (initial test of choice), elevated T4, elevated T3 (if TSH and T4 are inconclusive) Radioactive T3 uptake (testing TBG) - - if TBG is fully bound by T4, T3 will bind to resin administered. This test helps to differentiate between elevations in thyroid hormones due to increased TBG from true hyperthyroidism hyperthyroidism = ( T4 (all TBG sites will be bound by T4, so radioactive T3 uptake will increase) pregnancy = high TBG (more binding sites available for T3, so radioactive uptake will decrease) - - TBG is also increased by liver disease, OCPs, and ASA Tx: Pharmacologic: Thionamides: methimazole and propylthiouracil (PTU) inhibit thyroid hormone synthesis. PTU also inhibits conversion of T4 to T3. -blockers (propanolol): acute management of adrenergic Sx Sodium ipodate/iopanoic acid: lowers serum T4 and T3 with rapid improvement of disease; for acute management of refractory disease Radioiodine 131 (131I): destruction of thyroid follicular cells; MC for Graves disease; Major complication is hypothyroidism; CI in pregnancy and breastfeeding (cretinism). In pregnant patients PTU is preferred. Surgical subtotal thyroidectomy in 1% of patients due to high risk of permanent hypothyroidism, recurrent hyperthyroidism, and recurrent laryngeal nerve palsy. Reserved for large goiters or allergy to Rx Graves disease: Start with methimazole with -blocker ( taper -blocker after 4-8 weeks ( continue methimazole for 1-2 years ( measure TS IgG at 12 months ( if absent, D/C treatment ( if relapse, resume methimazole for 1 year or consider (131I). Thyroid Storm Life-threatening complication of thyrotoxicosis (hyperthyroidism) that is usually precipitated by infx, DKA, or stress with a mortality rate of up to 20% S/S: Marked fever, tachycardia, agitation, psychosis, confusion, GI Sx Tx: IVF, cooling blankets, glucose, PTU q2h followed by iodine to prevent T3/T4 release, -blockers to control HR, dexamethasone to prevent peripheral conversion of T4 to T3 and for adrenal support Hypothyroidism Etiology: Primary (MC): failure of the thyroid to produce sufficient T3/T4. Hashimoto s disease (chronic thyroiditis) and iatrogenic (radioiodine tx, thyroidectomy, Rx - - lithium) Secondary (pituitary disease - low TSH) and Tertiary (hypothalamic disease low TRH) - - both associated with low free T4 and low TSH. Subclinical Hypothyroidism: increased TSH maintains T4 level at normal range. Treated only when pt develops goiter, hypercholesterolemia, sx of disease, or significantly elevated TSH (>20 uU/mL) Sx: fatigue, weakness, lethargy, menorrhagia, slight weight gain, cold intolerance, constipation, slow mentation, muscle weakness, depression, diminished hearing Signs: dry skin, coarse hair, hoarseness, thick puffy features, non-pitting edema, CTS, slow DTRs, loss of lateral eyebrows, bradycardia, goiter Dx: High TSH level, low TSH (2), low free T4, increased antimicrosomal Ab in Hashimotos disease, elevated LDL with low HDL, mild normocytic anemia Tx: Levothyroxine (Synthroid) - - synthetic T4. Takes effect within 2-4 weeks. Given qAM, indefinitely with continued monitoring of TSH level. Thyroiditis Subacute / Granulomatous (viral): transient hyperthyroidism due to leakage of hormone from inflamed gland, followed by euthyroid state, then a hypothyroid state painful, tender gland that may be enlarged Dx: low radioiodine uptake due to the inability of damaged follicular cells to trap iodine. Low TSH, high ESR Tx: NSAIDs, ASA, corticosteroids (if severe pain) Recovery of thyroid fxn within a few months to 1 year Subacute lymphocytic (silent thyroiditis): transient, 2-5 month hyperthyroid state that may be followed by a hypothyroid state. Low radioactive iodine uptake (compared to high uptake in Graves). Chronic lymphocytic (Hashimotos): MCC of AI thyroid disorder; F>M S/S: goiter, hypothyroid sx (late) Dx: normal thyroid fxn tests, antithyroid Ab (antiperoxidase, antithyroglobulin) Tx: Synthroid Fibrous (Reidels thyroiditis): fibrous tissue replaces thyroid tissue, creating a firm thyroid. Treatment often involves surgery, and Synthroid if pt is hypothyroid. Thyroid Nodules/ Thyroid Cancer General Characteristics Risk factors: head and neck radiation (during childhood), Gardners syndrome and Cowdens syndrome for papillary cancer, MEN II for medullary cancer Types Papillary carcinoma (70-80%) least aggressive - - slow growth & spreading spreads via lymphatics in neck; freq. metastasizes to cervical LN; distant metastasis is rare positive iodine uptake MC to develop after radiation exposure (postradiation cancer) Tx: lobectomy with isthmusectomy total thyroidectomy if tumor is >3cm, tumor is bilateral, tumor is advanced, or distant metastases present adjuvant Tx: TSH suppression therapy; RAI therapy for larger tumors Follicular carcinoma (15%) avidly absorbs iodine prognosis is worse that for papillary cancer, but is still slow growing spreads early via a hematogenous route (brain, lung, bone, liver) distant metastasis 20%; lymph node involvement rare Tx: total thyroidectomy with post-op iodine ablation Variant: Hrthles Cell Tumor More aggressive Spreads to lymphatics; does not take up iodine Tx: total thyroidectomy Medullary carcinoma (2-3%) 1/3 sporadic; 1/3 familial; 1/3 associated with MEN II (always screen for pheochromocytoma) produces calcitonin more malignant than follicular carcinoma survival of 10y Tx: total thyroidectomy; RAI therapy unsuccessful Anaplastic carcinoma (5%) highly malignant poor prognosis death within months (due to invasion of adjacent organs - - trachea, neck vessels) Tx: chemotherapy and radiation may provide modest improvement in survival Diagnosis Thyroid hormone level (frequently normal) Calcitonin level (if medullary carcinoma) Fine needle aspiration (FNA): test of choice for initial evaluation of thyroid nodule Accuracy: S & S 95%. Reliable for all cancers EXCEPT follicular  Thyroid Scan (radioactive iodine) supplemental; performed if FNA is indeterminate graphic representations of the distribution of iodine hot (hyperfunctional) - - ( accumulation of RAI warm (normally functioning) cold (hypofunctional) - - ( accumulation of RAI limited to pt whose FNA biopsy results suggest neoplasm - - cold lesions require thyroid lobectomy Thyroid U/S differentiates a solid from a cystic nodule; most cancers are solid can identify nodules 1-3mm in diameter cystic masses >4cm in diameter are nonmalignant cannot distinguish between benign and malignant thyroid nodules Diseases of the Pituitary Gland Pituitary adenomas (10% of IC neoplasms) Usually benign; microadenoma (<10mm) and macroadenoma (>11mm) S/S: Hypersecretion GH acromegaly or gigantism ACTH Cushings disease TSH - hyperthyroidism Hypopituitarism: GH deficiency and hypogonadotropic hypogonadism Parasellar Mass effects H/A, bitemporal hemianopsia. Dx: MRI, pituitary hormone levels Tx: transsphenoidal surgery (except in prolactinomas); radiation therapy, medical therapy Hyperprolactinemia Etiology: Prolactinoma (MC adenoma), medications (psych, H2 blockers, estrogen), pregnancy, RF, suprasellar mass lesions, hypothyroidism, idiopathic S/S: Men: hypogonadism, decreased libido, infertility, impotence, galactorrhea, gynecomastia, parasellar effects (M>F) Women: Premenopausal: irregular menses, anovulation/infertility, decreased libido, dyspareunia, vaginal dryness, risk of osteoporosis, galactorrhea Postmenopausal: parasellar S/S Dx: elevated serum prolactin, pregnancy test and TSH levels, CT/MRI Tx: treat the underlying cause, bromocriptine (D-agonist) for 2 years, Cabergoline may be better tolerated, surgical intervention (high recurrence rate) Acromegaly Broadening of the skeleton due to excess GH after epiphyseal closure (gigantism if before) S/S: Growth promotion: soft tissue and skeleton overgrowth, coarsening of facial features, large hand and foot size, organomegaly, arthralgia, hypertrophic cardiomyopathy Metabolic disturbances: glucose intolerance/DM, hyperhydrosis Parasellar S/S: H/A, bitemporal hemianopsia (sup. growth), cavernosus sinus compression (lateral growth), sphenoid sinus invasion (inf. growth), HTN, sleep apnea Dx: IGF-1 (somatomedin C), failure of oral glucose suppression test to suppress GH, MRI, GH levels are too variant to be considered in dx Tx: transsphenoidal resection, radiation therapy if IGF-1 remains elevated after surgery, Octreotide to suppress GH secretion Craniopharyngioma (20-25% of tumors) Suprasellar region arising from embryologic remnants of Rathkes pouch causing visual defects, H/A, papilledema, and changes in mentation May cause hyperprolactinemia, DI, or panhypopituitarism Dx: MRI, calcifications on x-ray Tx: total or partial excision with or without radiation therapy Hypopituitarism Loss of hormones is unpredictable but usually lost in this fashion: LH, FSH, and GH first, followed by TSH and ACTH. Etiology: hypothalamic or pituitary tumor (MC), radiation therapy, Sheehans syndrome, infiltrative process (sarcoidosis, hemochromatosis), head trauma, surgery S/S: GH: growth failure Prolactin: failure to lactate ACTH: adrenal insufficiency TSH: hypothyroidism Gonadotropins: infertility, amenorrhea ADH (hypothalamic lesion): DI MSH: decreased skin and hair pigmentation Dx: low levels of target hormones with low or normal levels of trophic hormones, MRI Tx: hormone replacement, endocrinologist Diabetes Insipidus Two types: Central (MC): low ADH secretion Nephrogenic: ADH secretion is normal, but tubules are irresponsive to ADH Etiology: Central: idiopathic, head trauma Nephrogenic: hypokalemia, hypercalcemia, lithium, demeclocycline, pyleonephritis, congenital S/S: polyuria (5-15 L/day) that is colorless, thirst, polydipsia, hypernatremia (mild) Dx: low specific gravity (<1.006) and low osmolality (<280-310 mOsm/kg) Vasopressin challenge: fluid is withheld and urine osmolality is measured every hour. Desmopressin 2g SC is then administered and urine osmolality is measured 1 hr later. If there is a response, Dx is Central DI (due to lack of ADH)! ADH level: low in CDI, normal/elevated in NDI Tx: Central: desmopressin (DDAVP) nasally/PO/INJ, Chlorpropramide (increased ADH secretion Nephrogenic: Thiazide diuretics (+ amiloride) deplete serum Na++, which leads to increased reabsorption of sodium and water in the proximal tubules so that less water reaches the distal tubules, decreasing urine volume. Medical ID bracelet SIADH (increased ADH) Excess ADH leads to water retention and excretion of concentrated urine, leading to hyponatremia and volume expansion WITHOUT EDEMA (due to natriuresis). Natriuresis occurs due to: ( in atrial natriuretic peptide (increases urine Na++ secretion) ( in proximal tubular Na++ absorption Inhibition of RAAS Etiology: neoplasms (lung, pancreas, prostate, bladder), CNS disorders, pulmonary disorders, ventilators with PP, meds (SSRIs, vincristine, oxytocin, morphine, DDAVP), postop (anesthesia, pain) S/S: Acute hyponatremia: brain swelling (( ICF) leads to lethargy, seizures, weakness, coma, death Chronic hyponatremia: asymptomatic, anorexia, N/V, brain shrinkage (ICF ( ECF) Dx: Dianosis of exclusion. Hyponatremia + inappropriately concentrated urine; plasma osm. <270 mmol/kg Low serum uric acid, low BUN/Cr, normal thyroid and adrenal fxn, excess ADH, absence of significant hypervolemia Water-load test: intake of water load with measurement of urine output hourly. Large urine output (>65% in 4 hrs) is likely SIADH. Tx: Asymptomatic: water restriction, NS + loop diuretics for faster results, Lithium carbonate or demeclocycline inhibit the effect of ADH on the kidney. Symptomatic: water restriction, isotonic saline. Rapid increase in serum Na++ may lead to central pontine myelinosis (replacement should not exceed 0.5 mEq/L per hour) Diseases of the Parathyroid Glands Hypoparathyroidism Etiology: head and neck surgery (thyroidectomy) S/S: cardiac arrhythmias, rickets/osteomalacia, increased neuromuscular irritability due to HYPOCALCEMIA [numbness/tingling, grand mal seizures, tetany (( DTRs, Chvosteks sign, Trousseaus sign)], basal ganglia calcifications, prolonged QT interval. Dx: hypocalcemia, hyperphosphatemia, low serum PTH, low urine cAMP Tx: IV calcium gluconate (severe), oral Ca++ (mild/moderate), vitamin D supplement (calcitrol) - - MUST BE ADMINISTERED WITH CAUTION DUE TO ENHANCED EXCRETION OF CALCIUM IN URINE ( NEPHROLITHIASIS [8.0-8.5 mg/dL] Pseudohypoparathyroidism: end-organ resistance to PTH - - hypocalcemia, hyperphosphatemia, high PTH, low urinary cAMP Primary hyperparathyroidism MCC of hypercalcemia Etiology: adenoma >>> hyperplasia >> carcinoma S/S: Stones: nephrolithiasis Bones: osteitis fibrosa cystica (brown tumors) ( ( risk of fx Groans: muscle pain/weakness, pacreatitis, PUD, gout, constipation Psychiatric Overtones: depression, fatigue, anorexia, insomnia, anxiety, lethargy Other: polydipsia, polyuria, HTN, shortened QT interval, weight loss Dx: hypercalcemia, elevated PTH, hypophosphatemia, hypercalciuria, elevated urine cAMP, chloride/phosphate ratio 33:1 (due to renal bicarb wasting from PTH), subperiosteal bone resorption (2nd and 3rd phalanges), osteopenia Tx: SURGERY (definitive): pt <50, decreased bone mass, renal problems, severe hypercalcemia, urine Ca++ >400mg in 24 hrs. hyperplasia: all 4 glands removed, with placement of a small amount of parathyroid tissue in the forearm muscle to retain parathyroid fxn. adenoma: complete resection of adenoma is curative carcinoma: remove tumor, ipsilateral thyroid lobe, and all enlarged LN Medical: fluids, furosemide to enhance Ca++ excretion Secondary hyperparathyroidism Elevated PTH with low serum Ca++ Caused by: CRF (MCC), vitamin D deficiency, renal hypercalciuria Tx: vitamin D, calcitrol and oral Ca++ in CRF with dietary phoshorus restriction Diseases of the Adrenal Glands Cushings Syndrome Cushings Syndrome: excess glucocorticoids (cortisol) from the adrenal gland Cortisol causes: (1) increased protein catabolism, (2) anti-insulin effects, (3) impaired immunity, and (4) enhanced catecholamine activity - - HTN! Cushings Disease: pituitary Cushings syndrome (increased ACTH) May have hyperpigmentation due to additional rise of MSH Etiology: Iatrogenic (exogenous steroids prednisone) ( androgens are absent due to suppression by steroids ACTH-secreting adenoma, leading to B/L adrenal hyperplasia ( androgen excess Adrenal adenomas/carcinomas Ectopic ACTH production (leading to cortisol release from adrenals without normal negative feedback loop) ( SCLC, bronchial carcinoid, thymoma S/S: truncal obesity, hirsuitism, moon facies, buffalo hump, purple striae on abdomen, acne, easy brusing, HTN, DM, hypogonadism, masculinization in females (androgen excess in CD), muscle wasting/weakness, osteoporosis, AVN of femoral/humeral head, depression/mania, increased infections Dx: Low-dose Dexamethasone suppression test - - 1mg at 11pm, measure serum cortisol at 8am levels >5, and especially >10, is indicative of Cushings syndrome order a high-dose dexamethasone suppression test to determine the cause results in decrease in cortisol levels if no suppression of cortisol, ectopic tumor is likely 24-hour urinary free cortisol level (values > 4x normal) ACTH level once Cushings has been diagnosed low: adrenal tumor, hyperplasia high: pituitary adenoma, ectopic tumor CRH stimulation test IV if ACTH increases (positive response), then Cushings disease is the Dx if no response, then consider ectopic tumor or adrenal tumor Tx: Iatrogenic: taper glucocorticoid Pituitary: transsphenoidal ablation of pituitary adenoma Adrenal adenoma/carcinoma: surgery Pheochromocytoma Produce, store, and secrete catecholamines 90% in adrenal medulla (10% extra-adrenal) Rule of 10s: 10% familial, 10% bilateral (MEN II), 10% malignant, 10% multiple, 10% children, 10% extra-adrenal (MC = organ of Zuckerkandl @ aortic bifurcation) S/S: paroxysmal HTN, pounding H/A, profuse sweating, palpitations, anxiety, impending doom; hyperglycemia, hyperlipidemia, hypokalemia Dx: Urine screen: metanephrine, vanillylmandelic acid (VMA), normetanephrine Urine/serum Epi/NE ( Epi = adrenal or para-adrenal tumor nonadrenal tumors cannot methylate NE to Epi CT, MRI I-metaiodobenzylguanide scan (131I) taken up by tumor Tx: surgical tumor resection with early ligation of venous drainage to lower chance of adrenal crisis (catecholamine release) -blockers (phenoxybenzamine) Primary hyperaldosteronism Excess production of aldosterone by adrenals independent of RAS, leading to Na++ retention (HTN) and K+ loss (Hypokalemia), as well as H+ loss (metabolic alkalosis) Etiology: adrenal adenoma (Conn s syndrome), adrenal hyperplasia, adrenal carcinoma S/S: HTN, H/A, fatigue, weakness, polydipsia & nocturnal polyuria (hypokalemia), NO PERIPHERAL EDEMA Dx: Plasma aldosterone : renin ratio = 30:1 Saline infusion test (definitive) should decrease aldosterone levels to <8.5 ng/dL, which is not seen in this disorder (> 8.5 ng/dL) To Diagnoise Cause: Adrenal venous sampling for aldosterone levels: High on one side indicates adenoma. High on both sides indicates hyperplasia RAS stimulation test: measurement of serum aldosterone after recumbency or upright positions CT/MRI of adrenals, iodocholesterol scanning, arteriography/venograpy Tx: Adenoma: adrenalectomy Bilateral hyperplasia: spironolactone Adrenal Insufficiency Etiology: Primary adrenal insufficiency (Addisons disease MCC is TB): idiopathic, iatrogenic (B/L adrenalectomy), metastatic disease (lung, breast) - - HIGH ACTH! Secondary adrenal insufficiency: long-term steroid therapy leads to low release of cortisol due to suppression of ACTH and CRH - - LOW ACTH! Tertiary adrenal insufficiency hypothalamic disease S/S: Lack of cortisol: anorexia, N/V, abdominal pain, weight loss, lethargy, confusion, psychosis, hypoglycema, orthostatic hypotension, hyperpigmentation (stimulation of ACTH and MSH by low cortisol), intolerance to physiologic stress Low aldosterone: seen in primary alone due to dependence on RAS, not ACTH Hyponatremia: hypotension, ( CO, ( renal perfusion, weakness, shock Hyperkalemia Dx: Decreased plasma cortisol level Low plasma ACTH in secondary Standard ACTH test (definitive for primary): administered IV with measurement of plasma cortisol at the end of infusion Primary: cortisol does not increase sufficiently Secondary: initially no response due to adrenal hibernation. After 4-5 days, adrenals normally respond. 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Usually precipitated by stress (trauma, infxn, surgery) and is fatal if untreated. Tx: IV fluids (D5NS), IV hydrocortisone, treat underlying cause Congenital Adrenal Hyperplasia 21-hydroxylase deficiency S/S: Decreased cortisol and aldosterone production leading to increased ACTH (causes hyperplasia) Precursors of cortisol and aldosterone build up and are transformed to adrogens (virilization) female infants: hermaphroditism with normal ovaries and uterus (treatable) male infants: no genital abnormalities Salt wasting form (severe disease): emesis, dehydration, hypotension, shock in the first 2-4 weeks of life, Hyponatremia and hyperkalemia (low ald.), hypoglycemia (lack of cortisol) Dx: high serum 17-hydroxyprogesterone Tx: cortisol and mineralocorticoids to shut off excess ACTH secretion; early correction of female genital abnormalities FINE-NEEDLE ASPIRATION This is the only test that can differentiate between benign and malignant nodules! Findings: Probable cancer (15%): surgery indicated Indeterminate (19%): thyroid scan should be performed; 20% are found to be malignant - - surgical resection indicated Benign (66%): observe for 1 year, then F/U with U/S Follicular neoplasm: surgery is recommended because it is difficult to distinguish between benign and malignant follicular cells on histology. NODULES Cold: - Increased iodine uptake = hypofunctioning nodule - Significant risk of malignancy (20%) - 70-90% are cold, and most of those are benign - scanning may indicate a greatly reduced risk of malignancy in a nodule that is warm or hot, but it does not yield much additional information in a nodule that is cold. 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