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Adrenal 1


Aldosterone made in: zona glomerulosa
Aldosterone function Most important mineralcorticoid. Part of RAAS. Reabsorption of Na & excretion of K+. Prevention of hypovolemia & hyperkalemia
Cortisol function intermediary metabolism (eg, counters fx of insulin). Vascular tone. Water balance. Anti-inflammatory
Cortisol level highest when? in AM; in stress & exercise
Primary AI (AKA Addison dz) involves: all 3 zones of adrenal gland (potential insufficiency of cortisol & aldosterone)
Addison dz: DDx can be narrowed by: considering the abruptness of disease onset
Primary AI: abrupt onset: etiology Adrenal hemorrhage, necrosis, thrombosis; meningococcal sepsis (Waterhouse-Friderichsen Syn); pseudo; coag dz; mets ca w/ bleed
Primary AI: slow onset: etiology Auto-immune Adrenalitis; infxs Adrenalitis; Mets ca; congenital Adrenal Hyperplasia (CAH); Adrenomyeloneuropathy
Primary AI: clinical findings Hotn & hypoglycemia. Hyperpigmentation (2/2 XS ACTH). Salt craving; low Na & high K. NAGMA. Vitiligo, pallor. Autoimmune thyroid dz. CNS sx in adrenomyeloneuropathy.
Secondary AI (slow onset): etiology ACTH deficiency 2/2: Pit tumor / surgery / rad; craniopharyngioma; Megace; LT glucocorticoid tx (sudden D/C); sarcoidosis; hypothalamic tumor
AM cortisol results: >18: r/o AI; <3: R/I AI; btw this range: need dynamic testing
ACTH stim test 250 mcg Cosyntropin; measure cortisol before & 30 & 60 min after injxn; pre or post >18: R/O AI
Adrenal Insufficiency (AI) labs AM cortisol (low). ACTH stim (low). Low aldosterone. Plasma ACTH (>100: primary AI) (normal: 5-45)
Adrenal crisis tx Tx HYPOTENSION w/ volume (2 to 3 L of NS or D5NS); Give IV DEXAMETHASONE 4mg or IV HYDROCORTISONE 100mg TID (Dex preferred bc it won’t interfere w/ further dx testing & is long acting)
Chronic AI: maintenance therapy Hydrocortisone 20mg AM / 10mg PM; Dex; prednisone
Tx chronic primary AI: besides cortisol, must also tx insuff of: aldosterone: Fludrocortisone; check for postural HypoTN, orthostasis, serum K, renin; poss inc dose summer (inc persp Na loss) & dec dose in HTN (do not d/c altogether); NO K sparing diuretics for anti-HTN Rx
AI Prophylaxis: Steroids in Surgery Give pre-op hydrocortisone / continue 24 hrs; cut dose by 50% after first 24 h; cut dose by 50% each day until return to maint level (small procedures: give single dose of HC IV beforeprocedure)
Cushing syndrome: ACTH-independent: Adrenal lesion: exogenous source; Plasma ACTH level is low (< 5 pg/mL)
Cushing syndrome: ACTH-dependent: Plasma ACTH normal / high (>15 pg/mL). Ectopic ACTH or CRH production, adrenal ca/adenoma, pituitary adenoma (Cushing dz).
ACTH-dependent Cushing: to distinguish between ectopic & pituitary: 24h urine free cortisol. CRH-Stimulation test. LD & HD dex suppression. Petrosal sinus sampling. Octreotide scintigraphy to localize ectopic source. MRI
Cushing syndrome: tx Surgical resection: transnasal transsphenoidal resection of pituitary adenomas; adrenal tumor resection. Bilateral adrenalectomy (uncommon). Pharmacologic adrenal blockade; ketoconazole.
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
PCOS LH:FSH ratio >2.0 common
Androgen-secreting adrenal adenomas Rare; high serum androgen conc remain elevated despite Dex suppression
Androgen-secreting adrenal ca prevalence More common than adenomas
Androgen-secreting adrenal carcinomas usu > 5 cm at dx; Very high DHEA, DHEA sulfate; No response to HD Dex Suppression
Hirsutism / virilization: lab eval Serum testost (total & free); androstenedione (>1000: ovar adrenal neoplasm); DHEAS (>700: adrenal source of androgen xs; Need adrenal CT to detn if hyperplasia or ca)
Hirsutism / virilization: Imaging Pelvic Exam & US; Abd CT (esp adrenal glands/ fine cuts): adenoma / ca / hypertrophy
CAH Enzyme defects in adrenal steroid hor synth -> insuff cortisol +/-mineralocorticoid; classically with an assoc androgen excess
CAH: classical forms Salt-wasting form; Virilizing Syndromes
CAH: nonclassical forms Late-onset: women = hirsutism & menstrual irreg which can mimic PCOS; Men/boy: androgen excess can be asymptomatic
Hirsutism / virilization: Tx Stop any offending meds; Med tx options; Interventional tx options (Postmeno F can undergo lap bilat oophorectomy, if scans are nml; small hilar cell tumors of ovary may not be visible on scans
PCOS Tx options Oral Contraceptives (beware DVT); Metformin; Anti-androgen ( if NOT PG): Aldactone (spironolactone), Finasteride, Flutamide
Primary hyperaldosteronism: clinical findings Hypertension; Mx Sx (d/t hypokalemia): cramping, weakness, periodic paralysis. Often few clinical sx (Dx from lab abnormalities)
Primary hyperaldosteronism: labs BMP (low K, metab alkalosis). Serum renin & aldosterone ( Aldo/renin ratio >20 is suspicious). 24-hr urine aldost (high in setting of low renin (<5mcg/dL) suspicious). Saline-loading. 18-OH corticosterone
Primary hyperaldosteronism: labs: 18-OH corticosterone indicative of aldosterone producing adenoma (APA)
Primary hyperaldosteronism: imaging Abd CT (esp of adrenals); Adrenal vein sampling: for localization (cath of left an&d right adrenal veins & the IVC, looking for lateralization of elevated aldosterone level
Primary hyperaldosteronism: issues in evaluation Hold aldactone, CCB, ACEI. At least 150mEq of Na intake daily (to suppress aldosterone production)
Primary hyperaldosteronism: presenting forms APA (Conn dz, 65%). Bilateral hyperplasia of zona glomerulosa (35%). Primary adrenal hyperplasia. Adrenal carcinoma
Tx for aldosterone producing adenoma (APA): surgical (effective only in patients with unilateral disease). Angioplasty if RAS.
Primary hyperaldosteronism mgmt for poor surgical candidate Mineralcorticoid receptor antagonists: Spironolactone (DOC) or Eplerenone. CCB. ACEI
Pheochromocytoma = dz of adrenal medulla (site of catecholamine prodn)
Pheochromocytoma: 5 P’s pain; pallor (ortho hypoTN); palpitations; pressure (HTN); perspiration
Pheochromocytoma; rule of 10 10% of dz are: extra-adrenal; bilateral; familial; malignant; not assoc w/ HTN
Pheochromocytoma: Dx 24 hr urine (for Catecholamines & Metabolites: Metanephrines / VMA); Serum metanephrines/ plasma catecholamines; Imaging
Pheochromocytoma: Med mgmt Alpha adrenergic-blockade, then beta-blockade PRN. NEVER beta before alpha (may worsen HTN crises). CCB may be better tolerated than alpha-blockade.
Pheochromocytoma: Tx of choice Surgical resection is TOC. Need adequate a-blockade pre-op. Caution post-op comps (labile BP, hotn/shock, hypoglycemia)
Tertiary AI etiology low levels of corticotropin-releasing factor
Deficiency of which adrenocortical hormone is seen in secondary AI? Glucocorticoids only (esp cortisol). Aldosterone normal.
Cushing syndrome imaging Adrenal CT. CXR & MRI for ectopic site. DEXA
Hypercortisolism results in: decreased protein synthesis, increased protein catabolism, nitrogen wasting, glucose intolerance.
Cushing clinical features HTN, Wt gain/central obesity, moon face, buffalo hump, supraclavicular fat pads. Mx weak, fatigue. Poor wound healing, purple striae. Thin hair. Dysmenorrhea. Osteoporosis.
Cushing testing: late afternoon cortisol level: elevated level suggests lack of physiologic dip
Cushing Disease surgery Transphenoidal microsurgical removal (if proven Cushing dz)
Secondary hyperaldosteronism is due to: increased renin (eg, in RAS or renal hypoperfusion like CHF or hypovolemia)
Primary hyperaldosteronism MOA High aldosterone -> Na reabsorption -> volume expansion, HTN -> low K (2/2 ion exchange) -> AGMA
Pheochromocytoma patho tumor of chromaffin tissue from adrenal medulla -> secretes datecholamines (epi, norepi). May be 2/2 surgery, PG, exercise, TCAs, Reglan, opioids
Recurrent HA, HTN despiteBP meds, sweating, severe HA, glucosuria, abnormal urinary catecholamines & metanephrines = Pheochromocytoma
Group of familial disorders that affect multiple endocrine organs = MEN (multiple endocrine neoplasia)
MEN patho Auto dominant abnormalities -> hyperplasia or neoplasms
Types of MEN 1: Wermer syndrome. 2a: Sipple syndrome. 2b: Sipple tumors w/less preponderance of PTH hyperplasia +marfanoid & multiple neuromas
Wermer syndrome Affects PTH (90% of Wermer), pit adenoma, panc tumors (secrete insulin, gastrin, VIP, and serotonin.)
Sipple syndrome Thyroid (medullary carcinoma producing calcitonin), PTH, adrenals (pheo), and Hirschsprung dz
Wermer syndrome workup Measure PTH & Ca levels. Image pancreas & pituitary
Sipple syndrome 2a workup Measure PTH, urinary catecholamines, calcitonin. Image adrenals
Sipple syndrome 2b workup Same as for 2a plus eval for mucosal neuromas & marfanoid features
HyperPTH in MEN type 1: tx Cinacalcet
Paraneoplastic endocrine syndromes: most common ectopic hormones ACTH produced by SCLC & other carcinoids. ADH from SCLC, rarely prostate / cervical. PTH-related protein from squamous cell lung ca
Paraneoplastic endocrine syndromes: clinical features Cushing syndrome. SIADH. Hypercalcemia of malignant dz (in breast ca & myeloma, 2/2 local osteolytic features)
In pt with high Ca and low PTH, suspect: cancer (paraneoplastic syndrome)
Cushing pathology Pituitary adenoma (small basophilic intrasellar tumor). Adrenocortical adenoma (lipid-rich cells in cords). Adrenocortical hyperplasia. Ectopic (lung, thymus, pancreas)
Catecholamines (eg's) Epinephrine, norepinephrine, dopamine
Created by: Abarnard
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