Endo: Adrenal Disorders 1 Flashcards
(33 cards)
What controls secretion of the different adrenal hormones?
- Aldosterone secretion is regulated by angiotensin II
- Cortisol and androgen secretion is regulated by ACTH
- Norepi/epi are released in response to sympathetic stimulation
Describe the HPA axis, including negative feedback
- Hypothalamus releases CRH
- CRH stimulates the anterior pituitary to release ACTH
- ACTH stimulates adrenal gland to release cortisol and androgen
*Cortisol provides negative feedback onto hypothalamus and anterior pituitary
Name 2 stimulants for release of CRH from hypothalamus
Circadian rhythms
Stress
Where is the problem in primary and secondary adrenal insufficiency?
- Primary: problem is in adrenal cortex
- Secondary: problem is in pituitary or hypothalamus
Compare the levels of cortisol and aldosterone in primary and secondary adrenal insufficiency
- Primary adrenal insufficiency: low cortisol and low aldosterone
- Secondary adrenal insufficiency: low cortisol, normal aldosterone (ACTH is deficient but RAAS intact)
What is one infectious cause of primary adrenal insufficiency?
Tuberculosis
What is the most common cause of adrenal insufficiency?
Withdrawal of chronic glucocoticoids (secondary adrenal insufficiency)
Name 4 signs/labs unique to primary adrenal insufficiency
- Salt craving
- Vitiligo
- Hyperpigmentation
- Hyperkalemia
Name 3 electrolyte changes and one CBC change in adrenal insufficiency
- Hyperkalemia (primary only)
- Hyponatremia (primary only)
- Hypoglycemia
- Eosinophilia
What is the treatment for adrenal crisis?
IV Hydrocortisone
Why do patients with primary adrenl insuffiency have hyperkalemia and hyponatremia?
Lack of aldosterone (which normally stimulates kidneys to retain Na and secrete K)
Why do patients with primary adrenal insuffiency have hyperpigmentation
Increased synthesis of ACTH also produces excess Melanocyte Stimulating Hormone (POMC broken down into ACTH and MSH)
Primary has Pigmentation
What morning cortisol level is normal?
What diagnoses adrenal insufficiency?
Normal = 16-18
Adrenal Insufficiency = less than 5
Describe dynamic testing for adrenal insufficiency:
When is it used?
How does it work?
What question does it answer?
- Perform this test when morning cortisol is less than normal (16-18)
- Give synthetic ACTH (cosyntropin) and evaluate subsequent cortisol levels
- Cortisol under 20 indicates primary adrenal insufficiency or chronic secondary adrenal insuff
- This test answers: can your adrenals produce cortisol when stimulated?
Primary adrenal insufficiency
- Baseline serum cortisol will be
- Stimulated serum cortisol will be
- Plasma ACTH will be
Primary adrenal insufficiency
- Baseline serum cortisol will be less than 5
- Stimulated serum cortisol will be less than 20
- Plasma ACTH will be over 100
Secondary adrenal insufficiency
- Baseline serum cortisol will be
- Stimulated serum cortisol will be
- Plasma ACTH will be
Secondary adrenal insufficiency
- Baseline serum cortisol will be less than 5
- Stimulated serum cortisol will be less than 20
- Plasma ACTH will be low or normal
Compare the treatment of primary and secondary adrenal insufficiency
- Primary: give glucocorticoids and mineralocorticoids
- Secondary: give glucocorticoids only
What cells secrete renin?
What are 2 stimulators for renin release?
- Juxtaglomerular cells of kidney release renin
- In response to
- low renal perfusion
- low sodium concentration in the distal tubule
Describe the RAAS (5 steps)
- Renin released by JGA cells in response to decreased perfusion
- Renin cleaves Angiotensinogen (made in liver) into Angiotensin I
- Angiotensin I is cleaved into Angiotensin II by ACE in the lungs
- Angiotensin II stimulates aldosterone synthesis in adrenals
- Aldosterone causes Na reabsorption and K excretion in collecting duct principal cells
Name 3 causes of primary hyperaldosteronism
Which is most common
- Aldosterone-producing adenoma
- most common
- Bilateral adrenal hyperplasia
- Glucocorticoid remediable hyperaldosteronism
Describe the mechanism of glucocorticoid-remediable hyperaldosteronism.
What is the treatment?
- Aldosterone synthase gene gets translocated next to 11beta hydroxylase
- This causes aldosterone synthesis to be stimulated by ACTH
- Tx: Glucocorticoids to shut down ACTH
Name 4 labs indicative of hyperaldosteronism
- Resistant hypertension
- Hypokalemia
- Hypernatremia
- Metabolic alkalosis
Describe 2 tests for primary hyperaldosteronism
- Morning aldosterone/renin ratio greater than 20
- Suppression test
- Salt ingestion or give normal saline
- Aldosterone should get suppressed below 5
- Over 5 indicates primary hyperaldosteronism
Why do we perform adrenal vein sampling in people with hyperaldosteronism over age 35?
- Many older people have adrenal incidentalomas, so need to confirm that the mass seen on imaging is actually producing aldosterone (it may be unrelated)
