Adrenal Disorders (pt. 1, 2, 3) Flashcards
Paulson lectures
Zona glomerulosa secretes ____, such as ____.
- Function?
mineralocorticoids, such as aldosterone
- regulates BP and electrolyte homeostasis
Zona fasciulata secretes ____, such as ____.
- Function?
glucocorticoids, such as cortisol
- regulate stress response, immune system, metabolism
Zona reticularis secretes ____, such as ____.
- Function?
gonadocorticoids, such as androgens, progesterone, testosterone
aldosterone is synthesized from ____
cholesterol
production of aldosterone is stimulated by ____ and _____
- increase in K+
- angiotensin II secretion
aldosterone acts on convoluted tubules & collecting ducts to increase what?
- increase reabsorption of Na+
- increase excretion of K+ and H+
cortisol is released in response to what?
- stress
- low blood glucose
how does cortisol help increase blood glucose
stimulates gluconeogenesis
how does cortisol affect immune system
- decrease absorption of Ca2+ in GI
- decrease osteoblast production of new bones tissue
Didehydroepiandrosterone (DHEA)
- produced from cholesterol
- precursor of sex steroid hormone synthesis
- activates estrogen and testosterone
epinephrine is an agonist of ____ receptors
adrenergic
epinephrine effects
- increase HR & RR
- stimulates glycogenolysis & lipolysis
- muscle contraction
- vasoconstriction (vessels in GI, skin, kidneys)
- vasodilation (lungs)
_____ is a neurotransmitter and hormone that activates ____ receptors and plays a role in fight-or-flight response
Norepinephrine
- noradrenergic receptors
norepinephrine effects
- increase HR & BP
- decrease GI motility and urination
- triggers release of glucose from stores
- increase arousal/alertness. memory formation and retrieval
what are the classic findings of hyperaldosteronism
- difficult to control HTN
- hypokalemia, hypernatremia
- HA, vision impairment, muscle weakness, polyuria
some adrenal adenomas are nonfunctional, while other can secrete ____
- aldosterone (conn’s syndrome)
- cortisol (cushing’s)
- androgens (hyperandrogenism)
what test would you order if you suspect hyperaldosteronism
- PAC (plasma aldosterone conc)
- PRA (plasma renin activity)
High PAC:PRA = primary hyperaldosteronism
Low PAC:PRA = secondary hyperaldosteronism
hyperaldosteronism Tx
- adrenalectomy (unilat hyperplasia/carcinoma/adenoma)
- spirinolactone
- eplerenone
who is at higher risk of hypoaldosteronism
pts with DM, nephropathy, FHx, and NSAID/spirinolactone/heparin/beta-blocker use
clinical features of hypoaldosteronism
- hyperkalemia (without source)
- hypercloremic metabolic acidosis
- often asymptomatic
what labs would you order for hypoaldosteronism
- BMP (ele K, ele Cl, ele BUN/Crt)
- PRA and serum aldosterone
hypoaldosteron Tx
- primary = mineralocorticoid such as Fludrocortisone
- hyporen/hypoald = low K diet and diuretic (may use fludrocortison but can be bad for HTN)
primary adrenal insufficiency is also known as
Addison’s disease
causes for primary adrenal insufficiency
- autoimmune adrenalitis
- FHx
- infectious adrenalitis (TB, HIB, fungal)
- medication use
- metastases
- abrupt withdrawal of steroid Tx (suppresses HPA axis)
clinical features of primary adrenal insufficiency (Addison’s)
*both cortisol & aldosterone affected
- hyponatremia, hyperkalemia = Hypotension
- hyperpigmentation of skin & mm (d/t ele ACTH)
- salt craving
clinical features of secondary/tertiary adrenal insufficiency
- Hypoglycemia
- NO: hyperpigmentation, hyperkalemia, dehydration
clinical features of Addisonian crisis
- hypovolemic shock (hypotension)
- acute abdomen (abd TTP, N/V, fever)
- AMS
Addisonian crisis Tx
- aggressive IV fluids
- Hydrocortisone IV bolus (or Dexamethasone)
- Tx underlying cause (sepsis, hemorrhage)
DON’T DELAY TX WAITING FOR CORTISOL LVL
Primary adrenal insufficiency Tx
- Florinef + Hydrocortisone (MC & GC replacement)
GC given at different times to mimic nml endogenous cortisol levels
pheochromocytoma
- catecholamine producing tumor; commonly in adrenal medulla
- secretes mostly norepi, but also epi
pheochromocytoma pathophysiology
- arise from chromaffin cells (can also be from paragangliomas)
- stimulate alpha & beta receptors
pheochromocytoma triad
- HA
- sweating
- tachycardia
pheochromocytoma spells
- spontaneous
- from meds, exercise, increase abd pressure, anxiety, postural change
pheochromocytoma crisis (complications)
- ARDS
- acute HF
- pulmonary edema
- severe hypotension
- kidney & liver failure
- ICH
pheochromocytoma Tx
- alpha blocker (phenoxybenzamine)
- beta blocker
- increase salt and fluid intake
- surgical resection
how would you diagnose pheochromocytoma
- 24hr urine catecholamine/meta –OR– plasma fractionated metanephrines
- if elevated = CT or MRI
- if nml = repeat during a spell
how can multiple endocrine neoplasia be diagnosed
- clinical features (2+ of the associated tumors)
- familial pattern (associated tumor in a patient who has a 1st degree relative with syndrome)
- genetic testing
MEN1 (Wermer syndrome) affects what organs
- parathyroid
- anterior pituitary
- pancreas
MEN2a (Sipple syndrome) affects what
- parathyroid
- pheochromocytoma
- medullary thyroid carcinoma
MED2b affects what
- marfanoid body habitus
- pheochromocytoma
- medullary thyroid
MEN4 affects what
- parathyroid adenomas
- pituitary adenomas
- pancreatic neuroendocrine tumors
in association with gonadal, adrenal, renal, and thyroid tumors
congenital adrenal hyperplasia (CAH)
- genetic defect that decreases production of cortisol from its precursors
- AP secretes more ACTH to compensate
- increased ACTH during developmental years causes hyperplasia
(can lead to excess androgens and decreased aldosterone)
CAH clinical features
- skin hyperpigmentation
- Salt wasting = hyponatremia, hyperkalemia, dehydration, arrhythmia, vomiting
- short stature
- females with ambiguous genitalia and masculinization
CAH clinical features
- skin hyperpigmentation
- Salt wasting = hyponatremia, hyperkalemia, dehydration, arrhythmia, vomiting
- short stature
- females with ambiguous genitalia and masculinization
Chronic Tx for CAH
corticosteroids +/- mineralocorticoids (indefinitely)
to replace cortisol & aldosterone
CAH: Tx for salt-wasting crisis
- fluid rescusitation
- immediate hydrocortisone
- correct electrolyte imbalance
- mineralocorticoids replacement
ADMIT
clinical features of Cushing’s
- moon facies
- buffalo hump
- central obesity
- striae
- bruise easily
- hyperpigmentation
what is the first step in diagnosing Cushing’s
Determine increased cortisol levels
- Low-dose dexamethasone suppression test (overnight and 48 hour)
- late night salivary cortisol (11pm, 12am)
- 24hr urinary free cortisol excretion
what is the second step in diagnosing Cushing’s
Determine cause of increased cortisol
- Plasma ACTH (if low = adrenal tumor cause)
Tx of Cushing’s for:
- iatrogenic
- 1*
- cushing’s disease
- ectopic ACTH
- iatrogenic = taper off corticosteroid
- 1* = surgery
- cushing’s disease = transsphenoidal resection
- ectopic ACTH = surgery
