SACCM 82: Hypoadrenocorticism Flashcards
Describe the HPA axis
Hypothalamic-Pituitary-Adrenal axis
hypothalamus releases Corticotropin-releasing hormone (CRH) –> stimulates release of adrenocorticotropic hormone (ACTH) from the anterior pituitary –> stimulates production and release of cortisol from the adrenal cortex
What parts of the adrenal cortex produce and release cortisol?
zona fasciculata and reticularis
What part of the adrenal cortex releases aldosterone?
zona glomerulosa
Describe the steps of the RAAS
- Macula densa - (specialized cells in the distal portion of the thick ascending loop of Henle) - senses descreased filtrate delivery (specifically Cl-)
- Induces release of renin from the juxtaglomerular cells of the afferent arteriole
- Renin cleaves the circulating angiontensinogen to angiotensin I
- Angiotensin I is converted by endothelial angiotensin-converting enzyme (ACE) to angiotensin II
- Angiotensin II stimulates release of aldosterone from the zona glomerulosa
Name 3 things that can sitmulate aldosterone release
- Angiotensin II (RAAS)
- Direct response to hyperkalemia
- Minimal response to ACTH
Why do patients with secondary hypoadrenocorticism rarely show the classic addison’s electrolyte disturbances?
secondary means pituitary disfunction causes hypoadrenocorticism
zona glomerulosa only minimally responds to ACTH and more so to the RAAS system and hyperkalemia
List differentials for a low Na:K ratio
- hypoadrenocorticism
- parasitism
- kidney failure
- postrenal obstruction
- severe GI disease
- pregnancy
- body cavity effusions
also in EM book:
* CHF
* DM
Why do addisonian patients often present with inappropriately low USG?
sodium loss –> renal medullary washout (i.e., interstitial Na cc and therefore osmolality around the medullary collecting ducts is not sufficient)
What is a common acid base disturbance in addison’s disease and what causes it?
metabolic acidosis
from decreased renal tubular hydrogen ion excretion - would usually be enhanced by aldosterone
