Adrenal insufficiency

Question 1

Regulation of aldosterone

Answer 1

Increase K+ stimulates secretion – linear

Decreased Na+ and H2O volume stimulates production

• direct – sodium effect
• indirect – RAAS

Ang II increases production via increased aldosterone synthetase activity

Elevated Na+ can suppress secretion

ADH

Question 2

Primary hyperaldosteronism

Answer 2

Aldosterone secreting adrenal tumor – Conn syndrome

Triad:
Htn
Hypocalemia
Metabolic alkalosis

H/K exchanger -> urinary H+ loss, intracellular K+ out of cells

Low renin – negative feedback

Tx: surgical resection
Aldosterone antag to block receptor: spironolactone, eplerenone

Question 3

Secondary hyperaldosteronism

Answer 3

Elevated renin -> elevated aldosterone

Renal artery stenosis – decrease perfusion
Congestive heart failure – low EF -> decreased perfusion
Low protein states (cirrhosis, nephrotic sn) – low oncotic pressure -> edema, low vascular volume

Question 4

Primary adrenal insufficiency – Addison dz

Answer 4

MC autoAb attack cortex
Metastatic CA
TB
B/L hemorrhage – Waterhouse-Friderichsen Sn

Hypotension
Hyponatremia
Hyperkalemia
Generalized fatigue
Anorexia
Wt. loss
Skin hyperpigmentation – excess ACTH stimulates MSH receptors on melanocytes

Tx: mineralocorticoid and fludricordisone

Question 5

Waterhouse-Friderichsen sn

Answer 5

Acute primary adrenal insuffiency d/t adrenal hemorrhage

Severe meningococcal sepsis – Neisseria

DIC
Petechial rash

Question 6

Secondary adrenal insufficiency

Answer 6

No ACTH = no glucocorticoids

Still make aldosterone via renin system

No hyperkalemia
No hypotension
No hyperpigmentation
Weakness
Malaise
Wt loss

Question 7

Tertiary adrenal insufficiency

Answer 7

Interrupted CRH production from hypothalamus
d/t abrupt withdrawal of long term corticosteroids (MC)
-gradually taper to avoid

no hyperkalemia
no hypotension
-still making aldosterone