Endocrine Pt 2 (adrenal/parathyroid Flashcards
adrenal gland consists of
cortex and medulla
what does the adrenal cortex synthesize
glucocorticoids, mineralcorticoids (aldosterone), and adrogen
hypothalamus sends what to the anterior pituritary
corticotropin releasing (CRH)
after the anterior pituitary is stimulated by CRH what is released
corticotropin (ACTH)
ACTH stimulates the adrenal cortex to
produce cortisol
cortisol facilitates what conversion
NE to EPI in the adrenal medulla
cortisol induces what
hyperglycemia - refelcting gluconeogenesis and inhibiton of glucose uptak eby cells
together cortisol, aldosterone cause
Na+ retention and K+ excretion
what is pheochromocytoma
catecholamine secreting tumor that arises from chromaffin cells of the sympathoadrenal system
uncontrolled catecholamine release results in
malignant HTN, CVA, and MI
what is the cause of pheochromocytoma
precise cause unknown
90% are isolated
10% inherited
most pheo’s secrete what
NE:EPI ration 85:15 the inverse of normal adrenal secretion
some secrete higher levels of EPI, and rarely dopamine
how do malignant pheo’s spread
through venous and lymph systems
pheo attack triggers
can be spontaneous or triggered by injury, stress, or meds
symptoms of pheo attack
headache, pallor, sweating, palpitations, orthostatic Hypotension
what CV changes may occur with pheo
coronary vasoconstriction, cardiomyopathy, CHF, and EKG changes
diagnosis of pheos
24 hour urine collection for metanephrine and catecholamines
CT/MRI to localize tumor
preop for a pheo
alpha blockade to lower BP, decrease intravascular volume, prevent paroxysmal hypertenive episodes, allow sensitization of adrenergic receptors and decrease myocardial dysfunction
most common alpha blocker for pheo preop
phenoxybenzamine
noncompetitive alpha1 antag with some alpha2 properities
short acting, pure alpha1 blockers with less tachycardia
prazosin and doxazosin
tachycardia after alpha blockade should be treated with
BB
never give ______ BB before an alpha blocker - bc the blocking _______ receptors results in unopposed alpha agonism; leading to vasoconstriction and hypertensive crisis
nonselevcitve BB
B2 receptors
what is also used to control HTN with pheos
CCB
since calcium triggers catecholamine release from tumor and ecvess calcium entry into myoacrdial cells contributes to catecholamine mediated cardiomypoath
Cushing’s Syndrome aka
hypercortisolism
ACTH dependent Cushings is
inapproriately high plasma ACTH stimulating the adrenal cortex to produce excessive amounts of cortisol
acute ectopic ACTH is associated with small lung cell carcinoma
ACTH independent Cushings is
excessive cortisol productin by abnormal adrenocortical tissue that is not regulated by CRH and ACTH
what is usually the cause of ACTH independent cushings syndome
benign or malignant adrenocorticol tumors
symptoms of Cushing’s Syndrome
sudden weight gain, usually central with facial fat (moon) face, eccymoses, HTN, glucose intolerance, muscle wasting, depression, insomnia
Kahoot Q
diagnisos of cushings
24 hour urine demonstrating cortisol
Determining whether Cushing’s is ACTH dependent or independent requires reliable measurements of plasma ACTH using
immunoradiometric assays
The high-dose dexamethasone suppression test distinguishes
Cushings from ectopic ACTH syndrome
treatment for Cushings
transphenoidal microdenomectomy if microadenoma can be identified and resected
alternetive surgical resection for hypercortisolism
resection of anterior pituitary
other treatment for hypercortisolism
pituitary irradiation and bilateral total adrenalectomy
surgical removal of adreal gland is indicated for treatment
for adrenal adenoma or carcinoma
kahoot Q
preop for hypercortisolism
evaluate/treat BP, electroylte imbalance, and blood glucose
consider osteroposis positioning
Conn Syndrome is also known as
hyperaldoseteronism
primary hyperaldosteronism is
excess secretion of aldosterone from a functional tumor (aldosteronoma) that acts independent of physiologic stimulus
Conn Syndrome is also associated with
pheochromocytoma, hyperparaythroidism, or acromegaly
seconday hyperaldosteronism
presents when serum renin is increased, stimualting the release of aldosterone
symptoms of Conns
nonspecific - some are asymptomatic
HTN, hypokalemia, metabolic alkalosis
symptoms highly suggestive of hyper-aldosteronism
HTN and hypokalemia
T/F primary hyperaldo - plasma renin is suppressed
T/F secondary hyperaldo - renin activity is low
T) In primary hyper-aldosteronism, plasma renin activity is suppressed
F) In secondary hyper-aldosteronism, the plasma renin activity is high
long term licorice can cause a syndrome that mimic the features of hyperaldosteronism such as
suppresion of RAAS
hypokalemia
HTN
treatment for Conn’s Syndrome (6)
spironolactone
K+ replacement
Antihypertensives
diuretics
tumor removal
possible adrenalectomy
HyperK+ in the absence of renal insufficicency suggests
hypoaldosteronism
hyperK+ can be enhanced with
hyperglycemia
what form of acidosis is common with hypoaldosteronism
hyperchloremic metabolic acidosis
what symptoms may also be present with hypoaldosteronism
heart block secondayr to HyperK+, orthostatic Hypotension and hyponatremia
lack of aldo secretion reflects
congentitial deficiency of aldo synthesase or hyporenimeia caused by defects at the JGA or ACE-Is
hyporeninemic hypoaldo occurs in patients above 45 with
CRF or DM
Indomethacin induced prostaglandin deficiency is a (reversible or irreversible) cause
reversible cause
treatment for hypoaldo includes
liberal Na+ intake and dialy fludrocortisone
addison’s disease
adrenal glands unable to prodice enough glucocorticoid, mineralocorticoid and adrogen hormones
how much destruction of the glands need to be destroyed before signs appear in adrenal destruction
> 90%
secondary adrenal insufficency
hypothalamic-pituitary disease or supression leading to failure in the production of CRH or ACTH
with secondary adrenal insufficiency what is the deficiency
glucocortoid
most cases of adrenal insufficency are iatrogenic caused by
pituitary surgery irradation, or use of synthetic glucocorticoids
diagnosis of adrenal insufficency
baseline cortisol < 20 mcg/dL and remain <20 mcg/dL after ACTH stimulation
with ACTH stimulation - positive test demonstrates
poor response to ACTH and indicates an impairment of the adrenal cortex
absolute adreal insufficiency is characteristics vs relative adrenal insufficiency
absolute.. low baseline cortisol levels and positive result with ACTH stimulation
relative… higher baseline cortisol levels and positive result with ACTH stimulation
treatment for adrenal insufficiency
steroids
how many paraythroid glands are there
4
located bilateral of thryoid glands - has upper and lower poles
hypocalcemia stimualtes the release of
PTH
hypercalcemia suppresses
hormonal synthesis and release
PTH maintains normal plasma calcium levels by promoting the movement of Ca++
across the GI tract, renal tubules, and bone
primary hyperparathyroidism is caused by
benign parathyroid adenoma (90%)
carcinoma (<5%)
parathryroid hyperplasia
symptoms of hyperPTH
sedation, N/V, decreased strength and sedation, polyuria, renal stones, PUD, cardiac disturbances
diagnosis of hyperPTH
plasma Ca++, 24 hour urinary Ca++
treatment of hyperPTH
surgical removal of abnormal portions of the gland
what is secondary hyperPTH.. and a cause
compensatory response of the PTH glands to counteract a disease process (CRF) causing hypocalcemia
seldomly produces hypercalcemia
treatment for secondary hyperPTH
control underlying disease
normalize serum Phosphate concentrations with renal disease (PhosLow)
hypoPTH
when PTH is deficient or peripheral tissues are resistant to its effects
T/F hypoPTH is almost always iatrogenic
true - inadvertent removal od PTH glands as during thyroidectomy
what is pseudohypoparathyroidism
congenital disorder where PTH is adeqaute but the kidneys are unabel to respond to it
diagnosis of HypoPTH
Hypocalcemia < 4.5 mEq/L
iCa++ < 2.0 mEq/L
along with decreased PTH and increased phosphate
acute hypocalcemia with accidental removal of parathyroid during thryoidectomy may cause
inspiratory stridor = reflecting irritability of intrinsic laryngeal musculature
chronic hypocalcemia is associated with
fatigue, cramps, prolonged QT interval, lethargy, cataracts, SQ calcifications, thickening of skull, neuro deficits
common cause of hypocalcemia
chronic renal failure
