Week 5 (Exam 2) Flashcards
Acute adrenal crisis treatment
HYDROCORTISONE!
FLUIDS/GLUCOSE
treat hyperkalemia if needed
Confirmatory test of primary adrenal insufficiency
Cosyntropin (synthetic ACTH) stimulation test
11 B-HSD2 inhibitors
Too much active steroid
Glycyrrhizin (licorice), Carbenoxolone
Long-acting (greater than 36 hr) adrenal corticosteroid drugs
Betamethasone
Dexamethasone
Adrenal Destruction (Addison’s) causes
Autoimmune (most common)
X-Recessive (can mimic MS)
Tb!!
Waterhouse Friderichsen!!
Conn Syndrome
Unilateral aldosterone producing adrenal adenoma
40% have mut K channel, makes Metabolic Alkalosis
SAME: syndrome of apparent mineralocorticoid excess
11b-HSD2 deficiency (can also be caused by licorice)
Cortisol activates renal aldosterone. AD.
Child with HTN, Hypokalemia, Metabolic alkalosis
Low aldosterone and low renin
Low urinary free cortisone
McCune Albright Syndrome
Bilateral primary adrenocrotical hyperplasia
Polycystic fibrous dysplasia, cafe-au-lait spots, endocrine hyper function from multiple organs
MEN2b symptoms
Mucosal Neuromas Marfanoid Body Habitus Medullary Thyroid CA Pheochromocytoma (Gain of function RET)
Low serum ACTH in setting of low serum cortisol
Secondary adrenal insufficiency
Alabster skin: decreased pigmentation secondary to decreased secretion of a-MSH
Inherited adrenal unresponsiveness to ACTH (Addison’s) causes
Familial glucocorticoid deficiency (AR): Pigmentation
Isolated cortisol def., Mineralocorticoid normal, ACRH r.
AAA (Allgrove) Syndrome: mut ALADIN protein
Alacrima, achalasia, adrenal insuffiency, neuro disorder
Eplerenone
Mineralocorticoid receptor antagonist mainly
Tx HTN and prevents CV events
Cleared by P450(CYP3a4), eliminated 3-6 hours
Steady state within 2 days
Adverse: Hyper-K and increased creatinine
Mitotane
Can treat adrenal cortical carcinoma
Treatment for 21-hydroxylase (congenital adrenal hyperplasia) deficiency
Hydrocortisone
Fluids/Glucose
Get K levels down
MEN1 symptoms
Pituitary adenoma
Parathyroid Hyperplasia
Pancreatic Tumors
(Loss of function MEN1)
Distinguish primary vs 2/3 addisons
1: Hyperpigmentation, Hyper-K, responds to metyrapine
2/3: No hyperpigmentation, normal K, No ACTH response to metyrapine
3: ACTH response with CRH
Pheochromocytoma vs Paragangliomas
Pheochromocytoma: From adrenal medulla, secrete Epi and nor-epi
Paragangliomas: often metastasize, secrete nor-epic or nothing