Adrenal Gland Physiology Flashcards
The cortex is divided into four zones: _____________.
zona glomerulosa (outermost), zona fasciculata, zona reticularis, and medulla (innermost)
The mineralocorticoids are produced by which layer of the adrenal cortex?
Zone glomerulosa (outmost)
The glucocorticoids are produced by which layer of the adrenal cortex?
Zona fasciculata (second-most superficial)
The sex hormones are produced by which layer of the adrenal cortex?
Zona reticularis (third from the surface)
Epinephrine is made by the _____________.
adrenal medulla
Trace the adrenal chemical pathway.
Cholesterol
Pregnenolone (which gets converted to aldosterone)
17-OH pregnenolone (which gets converted to cortisol)
Dehydroepiandrosterone (which gets converted to sex steroids)
More than 90% of cortisol circulates _____________.
bound to cortisol-binding globulin (CBG)
Cortisol receptors are ______________.
Hsp90, which are cytosolic
What metabolic effects does cortisol have?
Increases gluconeogenesis Increases glycogenolysis Increases hormone-sensitive lipase, leading to release of FFAs Centripetal redistribution of fat Protein breakdown
What hematologic effects does the hormone secreted by the zona fasciculata have?
It (cortisol) increases RBC production, so excess cortisol can lead to polycythemia and deficient cortisol can lead to anemia.
Increased cortisol leads to _____________ collagen synthesis.
decreased (by inhibited fibroblast proliferation)
Why does Cushing’s syndrome lead to osteoporosis?
Cortisol is a vitamin D antagonist.
By what ways does cortisol inhibit the immune system?
- By inhibiting phospholipase A2, cortisol counteracts inflammation and vasodilation. Without vasodilation, leukocytes cannot get to infected tissues.
- By inhibiting fibroblast proliferation, infections are less containable.
- Cortisol also prevents T-cell proliferation.
Cortisol inhibits the secretion of ____________.
CRH
ACTH is derived from _______________.
proopiomelanocortin (POMC)
The key regulator of ACTH is ___________.
cortisol
Addison’s disease results from _____________.
primary adrenal insufficiency
What lab findings are suggestive of Addison’s?
Decreased cortisol and aldosterone
Increased ACTH
Secondary hypocortisolemia results from ____________. What lab findings are suggestive of this?
failure of the pituitary to secrete ACTH.
Decreased cortisol and ACTH
Primary Cushing’s (also called Cushing’s syndrome) will present with what lab findings?
Increased cortisol and decreased ACTH
Pituitary Cushing’s (also called secondary Cushing’s or Cushing’s disease) leads to what lab findings?
Increased cortisol and ACTH
The adrenal medullary cells are also called ____________.
chromaffin cells
Which nerve stimulates adrenal release of epinephrine?
The splanchnic nerve
One of the key inhibitors of hormone-sensitive lipase is ____________.
insulin
Alpha-adrenergic receptors outnumber beta-adrenergic receptors on pancreatic __________ cells.
beta; hence, epinephrine tends to inhibit insulin release
Adrenal cholesterol is mainly attained by _______________.
LDL circulation
The zona glomerulosa lacks the enzyme ___________, so all the pregnenolone gets converted to aldosterone.
17-alpha-hydroxylase
The zona fasciculata contains the enzyme ____________, which is necessary for corticosteroid synthesis.
11-beta-hydroxylase
What happens in the most common adrenal enzyme defect?
21-hydroxylase deficiency leads to absent aldosterone and cortisol and increased testosterone
Testosterone and ____________ have similar effects, but testosterone is just much more potent. In females, however, _______________ is the major androgen.
adrenal androgen (x2)
Two things must be replaced in primary adrenal insufficiency: ____________________.
glucocorticoids and mineralocorticoids
Explain the pathogenesis of congenital adrenal hyperplasia.
Congenital absence of 21-hydroxylase and 11-beta-hydroxylase leads to decreased production of cortisol and aldosterone. ACTH increases as a result of low cortisol levels, leading to adrenal hyperplasia. All of the increased pregnenolone gets converted to testosterone which, in females, leads to virilization of the genitals.
The main distinction between these two is that in 11-beta-hydroxylase deficiency an intermediate (11-deoxycorticosterone) is produced that can act to increase BP and decrease [K+].
