Adrenal Disorders Flashcards
adrenal medulla
- inner part of adrenal gland
- source of catecholamines (epinephrine and norepinephrine); richly innervated, extension of sympathetic nervous system
adrenal cortex
-secretes steroid hormones
5 groups of steroid hormones
- BASED ON RECEPTOR BINDING SITES
- mineralocorticoids: aldosterone
- glucocorticoids: cortisol
- androgens: testosterone, DHEA
- estrogens: estradiol, estrone
- Progestins: progesterone
diseases of the adrenal cortex
- cort insuff: adrenal crisis, addison’s dz
- cort excess: cushing’s
- aldo excess: primary hyperaldosteronism
diseases of adrenal medulla
-pheochromocytoma –> the only clinically important dz of the medulla
adrenal insufficiency: primary vs. secondary
- low cort
- primary: low serum cort, high ACTH - adrenal gland is not responding to ACTH
- secondary: low serum cort, low ACTH - pituitary not responding to feedback
acute adrenal insufficiency
- adrenal crisis
- emergency! cort insuff
- usually seen with withdrawal from exogenous steroids; post-operatively or with systemic use for chronic insufficiency
- weakness, abdominal pain, fever, confusion, n/v/d, low BP, dehydration, increased skin pigment
chronic adrenal insufficiency
- Addison’s disease (uncommon)
- weakness, easy fatigability, anorexia, weight loss, low BP, small heart
- n/v/d, abdominal pain, muscle and joint pain, amenorrhea, sparse axillary hair, increased skin pigmentation (esp creases, pressure areas, nipples)
stress dosing
-before surgery, you give steroids to balance them
Primary adrenal insufficiency causes
- autoimmune dz (most common)
- adrenal infections and inflammation
- bilateral metastases
- after adrenalectomy
- adrenal hemorrhage or necrosis
- idiopathic
- drug-induced
- congenital disorders
secondary adrenal insufficiency causes
- acute interruption of prolonged glucocorticoid therapy (most common)
- acute adrenal crisis - shock syndrome (most common)
- pituitary or hypothalamic tumor
- pituitary irradiation, surgery or brain trauma
- pituitary infections, inflammation, hemorrhage or necrosis
lab findings for adrenal insufficiency
- CMP with high K, low Na, high Ca, high BUN
- CBC with mild anemia, neutropenia with lymphocytosis and eosinophilia (chronic)
- low plasma cort at 8am
- high ACTH in primary adrenal dz
test needed for dx of adrenal insufficiency
- cosyntropin stimulation test
- synthetic ACTH (250mcg) given parenterally; draw blood 30-60 mins later; failure of serum cort to rise is diagnostic –> bolus of ACTH should drive cortisol production but if it doesn’t then its diagnostic
- low cort and low ACTH = secondary or tertiary adrenal insuff
- low cort and high ACTH = primary adrenal insuff
tx of adrenal insufficiency
- replace cort with hydrocortisone (or other form)
- tx infections aggressively; stress dosing appropriate –> if they have an infection, you need to increase cort level so their body can fight it off
cushing’s syndrome
- clinical manifestations caused by excessive corticosteroids
- facial plethora, proximal myopathy, striae, easy bruising
- central obesity, muscle wasting, thin skin, hirsutism, purple striae, osteoporosis, HTN, poor wound healing, psych changes, HA, polyuria, polydipsia, acne, nephrolithiasis
- “moon face,” “buffalo hump,” supraclavicular fat pads, protuberant abdomen, thin extremities
- oligo/amenorrhea, impotence
cushing’s dz vs syndrome
- dz = hypercort due to ACTH hypersecretion from pituitary (most common)
- syndrome = hypercort due to any cause
lab findings for cushings syndrome
- impaired glucose tolerance and insulin resistance, hyperglycemia, hypokalemia, normal Na on CMP
- leukocytosis, lymphocytopenia on CBC
cushing’s syndrome first line tests for diagnosis
- late evening salivary cortisol level
- 24 hr urine for free cort
- low-dose dexamethasone suppression test
- AT LEAST TWO OF THESE SHOULD BE ABNORMAL TO DIAGNOSE CUSHINGS SYNDROME
- once hypercortisolism is confirmed, plasma ACTH is ordered to find cause
low-dose dexamethasone suppression test
- standard screening tests to distinguish patients with Cushing’s disease (Cushing’s syndrome caused by pituitary hypersecretion of ACTH) from most patients with the ectopic ACTH syndrome (Cushing’s syndrome caused by nonpituitary ACTH-secreting tumors).
- overnight 1mg test: administer dex at 11pm to 12am, measure serum cortisol @ 8am –> most normal people have serum cort @ 8am of less than 2mcg/dl (55nmol/L)
who do you test for hypercortisolism
- pts with high likelihood of dz
- osteoporosis or HTN in young pts
- multiple progressive sxs of cushings
- unexplained severe fractures
- adrenal incidentalomas
- low index of suspicion: 1 test
- high index of suspicion: 2 tests
- exclude exogenous glucocorticoid use
testing ACTH to determine cause of Cushings syndrome
- suppressed ACTH (<5pg/mL) = ACTH independent Cushing’s syndrome –> adrenal CT/MRI
- intermediate ACTH (5-20pg/mL) –> CRH test –> no ACTH response = ACTH independent cushings. +ACTH response = ACTH dependednt cushings syndrome –> CRH stimulation and dex suppression tests, OR pituitary MRI
- normal to high ACTH >20pg/mL = ACTH dependent cushing’s syndrome –> CRH stimulation and dex suppression rests, OR pituitary MRI
MCC of cushings syndrome
cushings dz!!!
- originates from pituitary –> high serum cort, high ACTH
- 2nd MC = ectopic ACTH syndrome –> MOST COMMONLY FROM LUNG CANCER!!
- 3rd = Adrenal adenoma
primary hyperaldosteronism
- HTN and hypokalemia are classic presentation
- resistant HTN primary reason to consider this dx
- polyuria, polydipsia, muscular weakness
- elevated plasma and urine aldo levels, low plasma renin
- most common subtypes = aldo-producing adenoma and bilateral idiopathic hyperaldosteronism
- Tx: adrenalectomy, aldosterone antagonists (spironolactone or epelerenon = 1st line for meds), then potassium sparing diuretic (amiloride)
pheocromocytoma
- tumor in adrenal medulla - rare cause of HTN
- attacks of HA, perspiration, palpitations, tachycardia, anxiety
- HTN may be sustained, resistant to therapy or paroxysmal, esp in relation to stress