B5.034 Prework 1 Adrenal Mass Flashcards
3 layers of the adrenal gland
capsule
cortex
medulla
3 layers of the adrenal cortex
zona glomerulosa
zona fasciculata
zona reticularis
what is an adrenal incidentaloma?
an adrenal mass > 1 cm discovered serendipitously
4-6% prevalence, increases with age
what are the possible identifications of incidentalomas?
most are clinically non-hypersecreting benign tumors 5% autonomous cortisol production 5% are pheos 1% aldosterone producing adenomas 4% adrenal carcinomas 2.5% metastatic cancer
symptoms of pheo
basic triad: headache, sweating, palpitations
about half have sustained hypertension
most of the rest have paroxysmal spells
5% have neither
basic overview of pheos
tumor that produces excess catecholamines
equal sex incidence
increasing incidence with age
less than 0.1% of all patients with hypertension
rule of 10 for pheos
10% bilateral 10% extraadrenal (paragangliomas) 10% above the diaphragm 10% familial (really close to 30%) 10% malignant
lab diagnosis of pheo
elevated plasma fractionated metanephrines
elevated urinary fractionated catecholamines, metanephrines, and VMA
presence of adrenal mass on CT or MRI
special technique to image pheos
MIBG scan
pentetreotide
PET scan
treatment of pheo
pre-operative preparation with alpha blockers
beta blockers to prevent reflex tachycardia
surgical removal
volume replacement after surgery
what is the function of alpha blockers in pheo treatment
decrease chances of labile HTN
can increased chances of orthostatic HTN and reflex tachy, however (thus adding B blockers)
histo of a pheo
lots of Golgi in cells producing NE and epi
dark around nucleus
patient presentation with Cushings
fat pads moon face red cheeks bruisability thin skin poor muscle development poor wound healing striae pendulous adomen acne opportunistic infections
what is cushings disease
large spectrum of manifestations due to excessive glucocorticoid exposure either from the adrenal gland or exogenous
clinical findings in Cushings
truncal obesity IGT/diabetes in 20-60% hypertension in 70-80% hyperlipidemia coagulopathy osteoporosis in 30-50% depression in 50-80% hypogonadism central hypothyroidism decreases growth in children
diagnosis options in cushings
24 hr urinary cortisol more than 3x the upper limit
1 mg dexamethasone at 11 PM to 12 AM and measurement of serum cortisol at 8 AM, should be less than 1.8
late evening salivary cortisol
action of dexamethosone
substitutes for endogenous cortisol in suppressing ACTH release
pituitary MRI in the context of cushings
discrete adenoma will be visible in 35-65% of patients
10% of population 20-40 have incidental tumors of the pituitary with no symptoms
15% of patients with ectopic ACTH have abnormal results on MRI
when do you refer to surgery for cushings
unequivocal pituitary neoplasm on MRI >6mm in a patient without ectopic ACTH features
options for sources of cushings
pituitary: microadenomas, adenoma, hyperplasia
carcinoid tumor (usually lung)
adrenal: cortical adenoma, carcinoma, hyperplasia
what is inferior petrosal sinus sampling
bilateral simultaneous inferior petrosal sinus and peripheral venous sampling for ACTH levels before and after CRH stimulation
compare the ratios of ACTH in the petrosal sinuses to ACTH in the periphery after CRH
>3 = Cushings
ratio more even, carcinoma of the lung a possibility
treatment for cushings
curative treatment is transphenoidal surgery to remove the pituitary adenoma
when surgery is not an option, some meds can be given
ketoconazole mechanism
nonselective inhibitor of adrenal and gonadal steroids
blocks multiple enzymes in the cortisol pathway
ketoconazole adverse effects
headaches, sedation, nausea
potential hepatotoxicity
how do you treat cushings when all other options fail?
bilateral adrenalectomy
different causes of hypertension
primary hyperaldosteronism
secondary hyperaldosteronism
pheochromocytoma
essential hypertension
what is primary aldosterone excess?
high aldosterone, low renin
5-13% of patients with hypertension
20% of patients with resistant hypertension
causes of primary aldosterone excess
adrenocortical adenoma (Conn's syndrome) most common bilateral idiopathic hyperaldosteronism (IHA) due to micro or macronodular hyperplasia, 20-30%
secondary hyperaldosteronism
high aldosterone, high renin
usually due to renovascular hypertension, diuretic use, renin secretin tumors, or severe LV failure
clinical features of hyperaldosteronism
hypertension
hypokalemia > polyuria, nocturia, muscle cramps, occasional severe muscle weakness, paresthesia, tetany
more common in middle aged women
how to screen for hyperaldosteronism
plasma aldosterone: renin ratio in AM, can be on most hypertensive meds
ratio > 20 and plasma aldosterone >15 with suppressed renin
confirmatory test with oral salt loading or saline infusion
24 hour urine for aldosterone and sodium
describe a 24 hours urine study for aldosterone
24 hour urine for aldosterone and sodium
individual should be on a high salt diet
sodium excretion should be around 200
this amount of sodium should suppress aldosterone, so if aldosterone >12, there’s an issue
adrenal imaging results in hyperaldosteronism
if a solitary, unilateral adenoma >1 cm in a patient <40 y, proceed with laparoscopic resection
adrenal vein sampling indications
if CT is normal or nodules are <1 cm, bilateral, or patient is >40 yrs, adrenal vein sampling is the gold standard to determine is localized to one adrenal gland
treatment of hyperaldosteronism
decrease BOTH bp and aldosterone levels
laparoscopic resection will cure in 30-60% of unilateral adenomas
if surgery refused or bilateral hyperplasia, BP meds should include aldosterone receptor antagonists
aldosterone receptor antagonists
spironolactone
eplerenone
tumor marker for adrenocortical carcinoma
serum DHEA
potential effects of adrenocortical carcinoma
mass effect symptoms
symptoms related to excess glucocorticoid, mineralocorticoid, androgen or estrogen secretion
some typical causes for bilateral masses
generally not endocrine metastatic disease lymphoma infection hemorrhage
examples of endocrine bilateral adrenal masses
ACTH dependent cushings
bilateral pheo
bilateral primary hyperaldosteronism
