Endocrine
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| Water Deprivation Test: Central: | give AVP, later serum osm changes?
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| Hypercalcemia pathogenesis | accel bone resorption by osteoclasts (PTH, 1,25 (OH)D, IL-1, IL-6, TNF-alpha); enhanced GI absorption of Ca (vit D); hypercalcemia = eclipsed renal capacity to excrete Ca load (ie, hypercalciuria also present)
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| Hypercalcemia: causes | inc skeleton resorption (primary hyperPTH; malig); inc GI absorption (milk-alk syn); both inc skel resorp & GI absorption (granulomatous: sarcoid, TB, fungal)
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| Chvostek sx = | twitching of face and upper lip in response to tapping inferior to TMJ joint
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| Trousseau sx = | inflate BP cuff, leave it there; pt gets carpal spasm
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| Acute Hypocalcemia S/S | tetany, twitching, paresthesia; Chvostek sx; Trousseau sx; seizures; laryngo or bronchospasm; long QT; arrhythmia; hypotension
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| Chronic Hypocalcemia S/S | ectopic calcification (basal ganglia); EPS; parkinsonism; dementia; cataracts; abnml teeth; dry skin
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| Most common cause of hypocalcemia | surgically induced hypoPTH
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| Osteomalacia = | Defective bone matrix mineralization d/t: inadequate vit D/Ca & phosphorus; deficient mineralizn mechm in presence of normal Ca / phosphorus
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| Osteomalacia in childhood is: | rickets
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| Osteomalacia symptoms | diffuse bone pain (esp pelvis), waddling gait, mx weakness, fractures & pseudofractures (Looser’s zones) of long bones, ribs, pelvis
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| Osteomalacia: causes | Vitamin D def; Hypophosphatemia (inherited disorders); Mineralization disorders
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| Paget Disease = | Localized dysplastic bone formation/remodeling
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| Paget Dz: initiating lesion is: | inc bone resorption (giant multicellular osteoclasts); bone formation and mineralization is normal, though of IRREGULAR WOVEN TYPE
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| Paget Dz: most commonly affects which bones: | pelvis, femur, spine, skull and tibia
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| Paget Dz: Sx | pain, bowing, kyphosis, fracture, HA, MIXED HEARING LOSS (most common neuro sx); elevated alk phos (hallmark); bone turnover markers often elevated
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| GH deficiency seen in: | obesity & cortico-steroid therapy
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| 3 causes of pituitary dwarfism: | pit tumor (1/3); pit damage (1/3); Pure GH deficiency (1/3)
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| Most common disorder involving excess pituitary secretion | Prolactinomas
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| Central Diabetes insipidus: | Hypothalamic origin; ADH production or release is deficient
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| Nephrogenic Diabetes insipidus: | Kidneys fail to respond to normal/ high levels of ADH; 2/2 x-linked or Li tx, high K+ or low Ca+, or renal dz
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| H2O deprivation test: fx of exogenous ADH | Central DI: urine osmo will increase; Nephrogenic DI: urine osmo will not change
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| SIADH caused by: | excessive levels of ADH active material of non-pituitary origin
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| Osteoporosis risk factors | Personal hx of fx as adult; Hx of fx in 1st degree relative; current SMK; wt < 127 lb
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| Bone mineral density (BMD) values | T score: BMD > -1SD below YN = nml; severe osteo = BMD <-2.5
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| best predictor of bone fx risk | bone density (75-85% of variance in bone strength)
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| T-score: osteopenia | -1 to -2.5 SD below YN
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| Primary adrenal insuff: abrupt onset: etiology | Adrenal hemorrhage, necrosis, thrombosis; meningococcal sepsis (Waterhouse-Friderichsen Syn); pseudo; coag dz; mets ca w/ bleed
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| Primary adrenal insuff: slow onset: etiology | Auto-immune Adrenalitis; infxs Adrenalitis; Mets ca; congenital Adrenal Hyperplasia (CAH); Adrenomyeloneuropathy
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| Primary adrenal insuff: clin findings | Hyperpigmentation (due to xs ACTH); Salt craving; Hyponatremia; Hyperkalemia; Vitiligo, pallor; auto-immune thyroid dz; CNS sx in adrenomyeloneuropathy
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| Secondary/tert adrenal insuff: slow onset: etiology | Pit tumor / surgery / rad; Craniopharyngioma ; Isolated ACTH def; Megace (glucocorticoid-like action); LT g’corticoid tx; Sarcoidosis; Hypothalamic tumor
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| Hirsutism / virilization: etiology | Idiopathic (Familial); PCOS; Androgen-secreting adrenal adenomas or carcinoma; Ovarian tumors; Glucocorticoid resistance
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| Hirsutism / virilization: etiology: ACTH-dependent causes | Congenital Adrenal Hyperplasia; ACTH-dependent Cushing Syn
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| Androgen-secreting adrenal adenomas | Rare; serum androgen remain elevated despite Dex suppression
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| Androgen-secreting adrenal carcinomas | usu > 5 cm at dx; Very high DHEA, DHEA sulfate; No response to HD Dex Suppression
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| Congenital adrenal hypertrophy: etio | Enzyme defects in adrenal steroid hor synth => insuff cortisol +/-mineralocorticoid; classically with an assoc androgen excess
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| Congenital adrenal hypertrophy: classical forms | Salt-wasting form; Virilizing Syndromes
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| Primary hyperaldosteronism: clin findings | Hypertension; Mx Sx (d/t hypokalemia): cramping, weakness, periodic paralysis; Often few clinical findings at all (often suspected after lab abnormalities)
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| Primary hyperaldosteronism: issues in eval | S/b off Aldactone; CCB; ACEI (consider in-house eval); At least 150mEq of sodium intake daily (to suppress aldosterone prodn)
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| Primary hyperaldosteronism: presenting forms | Aldosterone-Producing Adenoma (Conn syndrome); Bilateral Hyperplasia of the Zona Glomerulosa (need remove both); Primary adrenal hyperplasia; Adrenal carcinoma
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| Cushing: lab dx | 24 hr urine cort; Dex suppression test; high PM cortisol
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| Asian M (15%), post high CHO or exercise, thyrotoxicosis => | hypokalemic periodic paralysis
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| Secondary hyperaldosteronism is: | more common than primary; usu d/t renal artery stenosis (curable by surg/angioplasty)
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