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Adrenal 2

Endocrine

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

 



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