Adrenal Gland Disorders Flashcards
(50 cards)
Adrenal gland hormones
glucocorticoids (cortisol)
mineralocorticoids (aldosterone)
androgens (DHEA)
catecholamines (EPI, NE)
Zones of the adrenal gland
glomerfulosa (aldosterone)
fasciculata (cortisol)
reticularis (androgens)
medulla (catecholamines, SS, substance P)
Regulation of aldosterone secretion
ATII
Potassium concentrations
Crotisol
fasciculata
increase blood glucose; metabolic effects
Regulation: ACTH, CRH
Androgens
reticularis
concerted to T, DHT, Estradiol
Regulation: ACTH, CRH
Catecholamines
medulla
increase BP, respiration, HR; constrict blood flow to GI tract
Regulation: preganglionic sympathetic neurons
Cortisol feedback
negative feedback to hypothalamus and anterior pituitary
Cortisol functions
stimulate gluconeogenesis, increase blood glucose decrease glucose uptake promote anti-inflammatory effects reduce bone formation increase proteolysis in muscle maintains normal BP decrease intestinal and renal calcium absorption, decreasing plasma calcium inhibits collagen formation
Cortisol release
released during night; peaks right when you wake up
Cushing syndrome
result of prolonged exposure to excess cortisol* and androgens
Features of cushing syndrome
reprod: mentrual irregularities (oligo or amenorrhea), hirsuitism, acne, increased libido
Derm: easy bruising, STRIAE, HYPERPIGMENTATION
Metabolic: glucose intolerance/hyperglycemia, CENTRAL OBESITY (moon face, buffalo hump)
CV: increased CV risk, HTN, increase VTE risk
Bone/MSK: Osteoporosis, proximal muscle wasting, weakness
Neuropsych: emotional lability, depression, anxiety
Cause of cushing
meds (prednisone)
tumor (pituitary adenoma)
ACTH dependent (80%): cushings disease = pituitary hypersecretion of ACTH; ectopic secretion of ACTH by non-pituitary tumor – ACTH and cortisol HIgh (F>M)
ACTH independent: latrogenic or factitious Cushing syndrome (adminitration of excessive cortisol); adenoma/carcinoma; pheochromocytomaa - High Cortisol, low ACTH
Dx of cushings
exclude exogenous glucocorticoids!
24-hour urinary free cortisol excretion***- gold standard
Late-night salivary cortisol
low-dose dexamethasone suppression tests
More: MRI- r/o pituitary tumor CXR - r/o lung mass as source of ACTH-secreting tumor Pelvic U/S: r/o ovarian mass CT abdomen: r/o adrenal tumor
Low-dose dexamethasone suppression test
1 mg oral dexamethasone administered at 11pm
serum cortisol levels measured at 8 am next morning
Elevated cortisol >5 mcg/dL = ABNORMAL***
if abnormal- highly suspicious for non-suppressible cortisol production from ACTH- indep etiology (adenoma/carcinoma)
Management of cushing
exogenous- taper to lowest dose
Pituitary adenoma - transsphenoidal resection
Adrenal tumor- adrenalectomy
adrenal hyperplasia - inoperable tumor, other malignacy -medical tx
Drugs for cushigns
Ketoconazole*** 1st line
Metyrapone (if keto ineffective this is added)
Mitotane- used to achieve “medical adrenalectolmy”
Aldosterone functions
increase BP* increase ECF increase tubular reabsorption of sodium promote excretion of potassium* water retention
Conn’s syndrome aka
Primary hyperaldostronism
Etiology of conn’s syndrome
Bilateral idiopathic adrenal hyperplasia (60%)
unilateral aldosterone-producing adenoma (APA) (30%)
Clinical features of conn’s
hypertension hypokalemia muscle weakness paresthesias h/a polyuria polydipsia
when to consider testing for conn’s
HTN + hypokalemia resistant HTN adrenal incidentaloma + HTN HTN <30 yo Severe HTN (>150 or >100) considering secondary HTN
Dx of Conn’s
Morning blood sample (PAC; PRA or PRC)
- PAC >10 + decrease PRA or PRC –> hypokalemia + PAC >20 = Conn’s; if no, do 24 hour urine, fludrocortison suppression testing OR saline suppression testin
- PAC <10 or PRA >1= surgically curable Conn’s is UNLIKELY
CT- r/o adrenal adenoma
Management of Conn’s
unilateral adenoma: surgical removal
Bilateral hyperplasia: mineralocorticoid receptor antagonist (SPIRONOLACTONE*** 1ST LINE) + other anti-hypertensives; monitor serum potassium, Cr, and BP frequently in first 4-6 weeks of therapy
Primary adrenal insufficiency aka
Addison’s