Adrenal 1 Word Scramble
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| Question | Answer |
| 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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