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Adrenal Pathophys
Adrenal Diseases
| Question | Answer |
|---|---|
| Layers of the adrenals from outside in | Zona Glomerulosa, Zona Fasiculata, Zona Reticularis, Adrenal Medulla |
| Where is aldosterone made? | In the zona glomerulosa. a mineralocorticoid |
| What does too much aldosterone cause? | High aldosterone --> high sodium --> high volume. Renin-angiotensin-aldosterone pathway |
| How does aldosterone work? | Stimulates renal tubule reabsorption of sodium and excretion of potassium |
| What is the function of Cortisol? | It is made in the zona fasiculata and reticularis. Counters the effects of insulin, is anti-inflammatory, and allows the body to respond to stress |
| Where are androgens made? | In the zona fasiculata and the reticularis |
| Androgen levels correlate with ____ levels | DHEA/DHEA-S (produced in large quantities by the adrenal gland, but the significance of DHEA is not understood) |
| Primary Adrenal Insufficiency is | dysfunction at teh level of the adrenal gland by a local lesion of disease process. Addison's disease |
| Secondary Adrenal Insufficiency is | From the level of the pituitary gland (inadequate ACTH secretion), or tertiary - from the level of the hypothalamus (not enough CRH secretion) |
| In Addison's disease, there is a deficiency in... | glucocorticoid as well as mineralocorticoid and androgen b/c it involves all 3 zones of teh adrenal cortex. Differential diagnosis can be narrowed by considering the abruptness of disease onset |
| Too much steroid, like in JFK's treatment of Addison's can cause what facial feature? | Fullness of the cheeks |
| Etiology of Primary Adrenal Insufficiency with abrupt onset | Adrenal hemorrhage, necrosis, thrombosis. Meningococcal sepsis, pseudomonas, coagulation disorders, metastatic cancer wtih bleed |
| Etiology of Primary Adrenal Insufficiency with slow onset | Auto-immune adrenalitis, infectious adrenalitis (TB is the main cause outside US), Metastatic cancer, Congenital Adrenal Hyperplasia (CAH), Adrenomyeloneuropathy (Debilitating neurological issues and adrenal insufficiency) |
| Primary AI: Clinical Manifestations | Hyperpigmentation (due to excess ACTH which is related to melanocyte stimulation), Salt Craving, Hyponatremia, Hyperkalemia, Vitiligo and pallor, auto-immune thyroid disease, CNS symptoms in adrenomyeloneuropathy |
| One of the clearest indication that patient has primary and not secondary AI | Hyperpigmentation; also electrolyte imbalance (low sodium, high potassium) |
| Slow Onset Secondary/Tertiary AI: Etiology | Pituitary tumor/surgery/radiation, craniopharyngioma, Isolated ACTH deficiency, Long-term glucocorticoid therapy (suppresses the axis), Megace (drug that has cortisol-like activity used in cancer patients. This helps them eat more), Sarcoidosis, tumor |
| Diagnosis of AI using AM cortisol values | > or equal to 18 is a normal result, rules out AI< or equal to 3 is a positive result, rules in AI. Between 3-18? Need dynamic testing. These rules apply to the outpatient not ICU b/c ICU has higher stress and thus different reference ranges |
| Describe the ACTH stimulation test | Grossly stimulate the adrenal gland with high ACTH (Cosyntropin - synthetic ACTH). Measure serum cortisol before, 30 and 60 min post injection. Can be given IM. Pre or post-cortisol > or equal to 18 rules out AI (primary and secondary |
| If you have ruled in AI by either a LOW AM cortisol or Subnormal ACTH response, what is the next step in diagnosis? | Check the plasma ACTH level |
| (plasma ACTH test) High ACTH: levels greater than 100 is consistent with | Primary AI |
| (plasma ACTH test) Normal ACTH level (between 5-45) effectively rules out | Primary AI |
| How do you treat an adrenal crisis? | Treat hypotension with Volume. 2-3L NS or D5NS. Give IV Dexamethasone or IV Hydrocortisone. Dexamethasone is preferred b/c it won't interfere with further diagnostic testing and it is long acting |
| Treatment of Chronic AI is | Glucocorticoid maintenance therapy (hydrocortisone, dexamethasone or prednisone) |
| Treatment of Chronic Primary AI | Aldosterone replacement. Fludrocortisone (generic of aldosterone) dosed daily. Dose may need to be adjusted depending on BP. If pt has high BP, decrease dose. Also, cause hyperkalemia. Dose may be higher in summer when NA lost to sweat |
| What should be avoided in the treatment of Chronic Primary AI with Aldosterone? | Do not use K sparing diuretics for anti-HTN Rx |
| AI prophylaxis steroids in surgery | Prior to surgery, give hydrocortisone 100mg IV once, continue Q8H for first 24 hours. Can reduce stress dose down to maintenance dose post-surgery |
| Cushing's syndrome | General term for hypercortisolism at any level including adrenal, ectopic (could be a lung tumor), or pituitary source |
| Cushing's disease | Refers specifically to an ACTH secreting PITUITARY ADENOMA with resultant cortisol secretion. |
| How do you estimate cortisol excess? | 24-hour urine free cortisol test, Low-dose dexamathasone (glucocorticoid, if normal, it should suppress the axis) suppression test, Elevated late evening serum cortisol (should be at its nadir). Remember, exclude exogenous glucocorticoids |
| What would be a source of exogenous glucocorticoids? | A patient who is applying a lot of topical hydrocortisone cream |
| After establishing cortisol excess what is the next step in diagnosis? | Establish if it is ACTH independent or dependent |
| If Cushing's syndrome is ACTH-independent suspect: | adrenal lesion, exogenous source. Plasma ACTH level is low (<5pg/mL) |
| If Cushing's syndrome is ACTH-dependent, suspect: | Ectopic production or pituitary adenoma (Cushing's disease). Plasma ACTH level is normal or high (>15pg/mL) |
| In ACTH-dependent Cushing's syndrome, in order to distinguish between ectopic vs pituitary, which tests should be performed? | CRH-Stimulation test, High-dose dexamethasone suppression, petrosal sinus sampling, Octreotide scintigraphy (to localize ectopic source), MRI |
| Cushing's syndrome Treatment | Surgical resection, transphenoidal microsurgical removal, bilateral adrenalectomy (uncommon), pharmacolgic adrenal blockade |
| Hirsutism | Increased hair growth on chin, upper lip, abdomen and chest. Acne also seen |
| Virilization | from androgen excess, menstrual irregularities, decrease in breast size, frontal balding, deep voice. PELVIC EXAM provides a lot of information |
| Hirsutism and Virilization Etiology | Idiopathic (Familial), PCOS, Androgen-secreting adrenal adenomas (tumor of cortex)or carcinomas, ovarian tumors, ACTH dependent causes: Cushing's syndrome, congenital adrenal hyperplasia, Glucocorticoid resistance |
| PCOS (polycystic Ovarian Syndrome) | LH:FSH ratio greater than 2.0 is common. 1/3 of nl women have polycystic ovaries on US. Not essential to dx. Clinical history is important: menstrual irregularity, adndrogen excess, hirsutism, Obesity and insulin resistance |
| Hirsutism and Virilization Etiology | Androgen-secreting adenomas: rare, slowAndrogen-secreting adrenal carcinomas: abrupt history, more common than adenomas, tumor usually greater than 5cm at dx, very high DHEA. No response to High-dose dexamethasone suppression |
| Lab evaluation of Hirsutism and Virilization | Serum Testosterone: total and freeAndrostenedione: Greater than 1000ng/dL implies ovarian adrenal neoplasmDHEA-S: high implicates adrenal source of androgen excess. Need adrenal CT to determine if hyperplasia or a carcinoma |
| Lab Evaluation of Hirsutism and Virilization | Amenorrhea: PCOS/Ovarian failure/extensive DDx, LH/FSH, Estradiol, Testosterone/DHEA |
| Hirsutism and Virilization Imaging | Pelvic Examination, Pelvic US, Abdominal CT with attention to the adrenal glands (adenoma, carcinoma, hypertrophy) |
| What is Congenital Adrenal Hyperplasia? | Enzymatic defects in the adrenal steroid hormone synthesis pathways leading to: inadequate cortisol +/- mineralocorticoid, classically with an associated androgen excess |
| Classical Forms of Hirsutism and Virilization | Salt-wasting, virilizing syndromes. |
| Non-Classical forms of Hirsutism and Virilization | Late-onset: women present with hirsutism and menstrual irregularity which can mimic PCOS, In men/boys, androgen excess can be asymptomatic |
| Hirsutism and Virilization Treatment | Stop offending medications, post menopausal women can undergo laparoscopic bilateral oophorectomy, medical treatment options |
| PCOS treatment options | Oral contraceptives (beware of DVT and other risks), Metformin, Anti-androgen (only if not pregnant): Aldactone (spironolactone), Finasteride, Flutamide |
| Primary Hyperaldosteronism Clinical Findings | Hypertension, Muscle symptoms (due to hypokalemia): cramping, weakness, periodic paralysis, Often few clinical findings at all |
| Primary hyperaldosteronism Lab series and Imaging | 24-hour urine aldosterone, Chem7, Serum renin and aldosterone levels, Saline-loading, CT scan of abdomen, 18-0H Corticosterone level, Adrenal vein sampling. Looking for high aldosterone and low renin to prove hyperaldosteronism. |
| Aldosterone inhibits ________ | renin |
| Lab findings of Primary Hyperaldosteronism | Hypokalmia, metabolic alkalosis, low renin, high aldosterone, 24 hr urine aldosterone elevated, CT may find solitary adenoma or carcinoma |
| Classic way to diagnosis Primary hyperaldosteronism | Adrenal vein sampling. Not the first step. Labs and radiology come first. Catheterization of left and right adrenal veins and the IVC, looking for lateralization of elevated aldosterone level |
| Prior to evaluation of Primary Hyperaldosteronism, what is required? | must be off anti-aldosterone meds (spirinolactone), preferrably off ACEI and CCB, at least 150mEq of sodium intake (don't want them to be low salt so the body appropriately makes more aldosterone) |
| Primary Hyperaldosteronism presenting forms | Solitary/unliteral aldosterone-producing adenoma (APA = Conn's syndrome: HTN, hyperaldosteronism and tumor), Bilateral, primary adrenal hyperplasia, adrenal carcinoma |
| Define Conn's syndrome | Triad of: HTN, hyperaldosteronism, and solitary/unilateraal aldosterone-producing adenoma |
| Primary Hyperaldosteronism Treatment | Aldosterone Producing Adenoma: surgical(only in unilateral disease)Medical Therapy: mineralocorticoid receptor antagonists, spirinolactone (DOC), Eplerenone. Amiloride no longer recommneded. CCB, ACEI (to control BP) |
| Drug of Choice in Hyperaldosteronism | Spirinolactone |
| Pheochromocytoma | Disease of the adrenal medulla |
| What does the adrenal medulla do? | Produces catecholamines: epinephrine, norepinephrine, dopamineSympathetic system: fight of flight responses |
| Pheochromocytoma Clinical Findings | Five P'sPain - headachesPallor - Orthostatic hypotension from impaired arterial and venous constriction responsesPalpitations - catecholamine response, heart racingPressure - HTNPerspiration |
| Pheochromocytoma Rule of 10s | 10% extra-adrenal, 10% bilateral, 10% familial (24%), 10% malignant (3-36%), 10% not associated with HTN |
| Classic findings of Pheochromocytoma | HTN, fainting spells, palpitations, sweating, headaches |
| Pheochromocytoma Diagnosis | 24 hours urine collection for catecholamines, catecholamine metabolites (metanephrines and Vanillylmandelic acid (VMA)). Plasma draw for free metanephrines may be a good screening tool. Imaging MRI |
| Pheochromocytoma Key points in evaluation | Check pt meds: acetominophen, bronchodilators, caffeine, coffee, labetalol, etc. Look for familial syndromes: MEN IIA, IIB, Von Hippel-Lindau, Von Recklinghausen (Neurofibromatosis type I) |
| Pheochromocytoma Pharmacologic Treatment | Pharmacologic: Alpha Adrenergic-Blockate first (phenoxybenzamine), Beta-blockade next if necessary (never start before alpha blockade b/c unopposed alpha-receptor stimulation can lead to worsened HTN crisis), CCB (better tolerated than alpha-blockade) |
| Pheochromocytoma Treatment | Surgical resection of adrenals is treatment of choice, need adequate alpha blockade pre-operatively, Watch for post-operative complications: labile blood pressure, post-resection hypotension/shock, hypoglycemia |
| What is the treatment of Choice for Pheochromocytoma? | Surgical resection of adrenals: may require open laparotomy, consider search of sympathetic chain |
Created by:
ltm12