Physio: Endocrine - Adrenal Medulla And Cortex

Front 1

What is the embryological origin of the adrenal medulla?

Back 1

neuroectoderm

Front 2

What is the embryological origin of the adrenal cortex?

Back 2

mesoderm

Front 3

What are the layers of the adrenal cortex (from outside to in), and what hormones do they each primarily secrete?

Back 3

Zona glomerulosa (mineralocorticoids-aldosterone)
Zona fasciculata (glucocorticoids-cortisol)
Zona reticularis (androgens-dehydroepiandrosterone(DHEA) and androstenedione)

Front 4

What is the first step in the biosynthetic pathway of steroid hormones? What factor stimulates this step?

Back 4

Cholesterol (via cholesterol desmolase) -> pregnenolone

Stimulated by ACTH

Front 5

What hypothalamic and a/p hormones regulate the release of glucocorticoids, androgens, and mineralocorticoids?

Back 5

ACTH and CRH (for glucocort and androgens)

for mineralocorticoids: depends ACTH (no a/p control), and is controlled separately by renin-angiotensin-aldosterone system

Front 6

What is the pattern of cortisol secretion (when is it highest/lowest?)

Back 6

pulsatile nature, diurnal pattern; oscillates with circadian rhythm (highest ~8am, lowest ~12am)

*is driven by the diurnal pattern of ACTH secretion (which in turn, is driven by CRH burst)*

Front 7

What are the effects of ACTH?

Back 7

stimulate cholesterol desmolase, up-regulates its own receptor, and when chronically increased, causes hypertrophy of adrenal cortex

Front 8

What negative feedback mechanisms are present for the secretion of cortisol?

Back 8

cortisol inhibits CRH release from hypothalamus and secretion of ACTH from a/p

Front 9

Pt is given a dexamethasone suppression test. Low dose does not suppress cortisol, but high does does. What might the disorder be?

Back 9

ACTH-secreting tumor

Front 10

Pt is given a dexamethasone suppression test. Neither low dose nor high dose suppresses cortisol. What might the disorder be?

Back 10

adrenal cortical tumor (secretes cortisol)

Front 11

Is aldosterone regulated by ACTH?

Back 11

yes, it is under tonic control by ACTH

Front 12

Pt becomes volume depleted. Describe the cascade that follows.

Back 12

Dec ECF -> dec perfusion pressure -> inc renin -> catalyzes angiotensinogin to angiotensin I -> (via angiotensin converting enzyme (ACE)) to angiotensin II -> stimulates corticosterone to aldosterone in zona glomerulosa -> inc Na r/a, inc K s/c -> inc ECF

Front 13

Pt becomes hyperkalemic. What is the hormonal response?

Back 13

K depolarizes adrenal cells, opens Ca channels, Ca rushes in, stimulates aldosterone s/c

Front 14

What are the metabolic effects of glucocorticoids (cortisol)?

Back 14

Overall, effects are catabolic and diabetogenic: stimulates gluconeogenesis, inc protein catabolism in musc and dec new protein synthesis (provides addnl AA to liver for gluconeo), inc lipolysis (addnl glycerol to liver), dec gluc utilization by tissues, dec insulin sensitivity of adipose tissue

Front 15

What happens to glucose levels in hypocortisolism? In hypercortisolism?

Back 15

hypocortisolism -> hypoglycemia

hypercortisolism -> hyperglycemia

Front 16

What hormone mediates the stress response?

Back 16

cortisol (glucocorticoids)

Front 17

What adrenocortical steroid is critical for survival during fasting?

Back 17

cortisol (glucocorticoids)

Front 18

What are the effects of cortisol on the immune system?

Back 18

Anti-inflammatory and immunosuppressive:
-induces synthesis of lipocortin, which inhibits phospholipase A2 (key for AA metabolism), thus inhibits precursor of leukotrienes and prostaglandins
-inhibit IL-2 and T cell proliferation
-inhibits release of histamine and 5HT from mast cells and platelets

Front 19

What are the vascular effects of cortisol?

Back 19

up regulates alpha-1 adrenergic receptors, required for vasoconstrictive response to NE

(hypocortisolism -> hypotension; hypercortisolism -> hypertension)

Front 20

What are the actions of mineralocorticoids (aldosterone), and what cell types mediate these effects?

Back 20

-principal cells of late distal tubule and collecting ducts -> inc Na r/a and K s/c
-alpha-intercalated cells of LDT and CDs) -> inc H s/c

Front 21

What role do adrenal androgens (DHEA and androstenedione) play in males?

Back 21

small role; converted to testosterone in testes (but most testosterone is synthesized de novo in testes)

Front 22

What role to adrenal androgens (DHEA and androstenedione) play in females?

Back 22

important for pubic and axillary hair, and libido

Front 23

What is adrenogenital syndrome? What are the sx?

Back 23

inc synthesis of adrenal androgens; masculinization of females, early hair development, and suppression of gonadal fn in males and females

Front 24

Sx: weight loss, weakness, nausea, hyperpigmentation, low bp, high K, metabolic acidosis, hypoglycemic upon fasting, dec pubic/axillary hair in females, high ACTH levels

What is the cause? What is the disorder?

Back 24

Low aldosterone, cortisol, and adrenal androgens

Primary adrenocortical insufficiency (Addison's Disease): autoimmune destruction of all zones of adrenal cortex

Front 25

What causes hyperpigmentation in Addison's disease?

Back 25

increased levels of ACTH from negative feedback (which contains the alpha-MSH fragment)

Front 26

What is the treatment for Addison's disease?

Back 26

Glucocorticoid and mineralocorticoid replacement

Front 27

Sx: weight loss, nausea, weakness, hypoglycemia, low ACTH levels

What is the cause? What is the disease?

Back 27

Insufficient ACTH levels (from failure of corticotrophs in a/p)

"Secondary adrenocortical insufficiency"

*no symptoms of hypoaldosteronism, no hyperpigmentation*

Front 28

Sx: hyperglycemia, central obesity, round face, supraclavicular fat, buffalo hump, muscle wasting, osteoporosis, striae, high bp, (and virilization & menstrual d/o's in women)

What is the cause? What is the disease?

Back 28

excessive glucocorticoids and adrenal androgens

Cushing's syndrome or Cushing's disease

Front 29

What is the cause of Cushing's syndrome?

Back 29

primary adrenal hyperplasia (spontaneous overproduction of cortisol) or exogenous glucocorticoids

Front 30

What is the cause of Cushing's disease?

Back 30

pituitary adenoma which causes hypersecretion of ACTH

Front 31

What test can differentiate between Cushing's syndrome and Cushing's disease? How will the results differ?

Back 31

dexamethasone suppression test

Cushing's syndrome (LOW ACTH): neither low nor high dose can suppress cortisol levels

Cushing's disease (HIGH ACTH): not low dose, but high dose can suppress cortisol levels

Front 32

What is the the treatment for Cushing's sydrome?

Back 32

drugs that block steroid biosynthesis (ketoconazole or metyrapone)

Front 33

What is the treatment for Cushing's disease?

Back 33

surgical removal of ACTH-secreting tumor

Front 34

Sx: hypertension, hypokalemia, metabolic alkalosis, decreased renin levels

What is the disturbance? What is the disease?

Back 34

aldosterone secreting tumor -> Conn's syndrome

Front 35

What is the treatment for Conn's syndrome?

Back 35

aldosterone antagonist (spironolactone), followed by surgical removal of aldosterone-secreting tumor

Front 36

How can symptoms of increased adrenal androgens, but decreased glucocorticoids and mineralocorticoids be explained?

Back 36

21 beta-Hydroxylase deficiency (a type of adrenogenital syndrome)

progesterone and 17-hydroxyprogesterone cannot be converted to the steroid intermediates that lead to mineralocort's and glucocort's. thus all steroid intermediates above block are shunted toward production of adrenal androgens

Front 37

Will ACTH levels be increased or decreased in 21 beta-Hydroxylase deficiency?

Back 37

increased (negative feedback effect of cortisol)

Front 38

How can sx of increased mineralocorticoids, but decreased adrenal androgens and glucocorticoids be explained?

Back 38

17 alpha-Hydroxylase deficiency

pregnenolone and progesterone cannot be converted to the steroid intermediates that lead to andrenal androgens and glucocort's. thus all steroid intermediates above block are shunted toward production of mineralocorticoids.

Front 39

Will ACTH levels be increased or decreased in 17 beta-Hydroxylase deficiency?

Back 39

increased (negative feedback effect of cortisol)

Front 40

What is the treatment for 21 beta-Hydroxylase deficiency?

Back 40

replacement of mineralocorticoids and glucocorticoids

Front 41

What is the treatment for 17 beta-Hydroxylase deficiency?

Back 41

replacement of glucocorticoids and aldosterone antagonist