Adrenal gland, continued (L6)

Question 1

What is the primary action of mineralocorticoids?

Answer 1

Promote sodium retention by the kidney

Question 2

Secondary result of sodium retention

Answer 2

Water retention

Question 3

Primary endogenous MC

Answer 3

Aldosterone

Question 4

11-deoxycorticosterone

Answer 4

Precursor of aldosterone that also has MC action

Question 5

Aldosterone synthase - location

Answer 5

Primarily located in the zona glomerulosa of the adrenal cortices

Question 6

Sites of action of aldosterone

Answer 6

Kidney
Colon
Salivary glands
Sweat ducts

Question 7

Aldosterone effects on the kidney

Answer 7

Primary target. Retains sodium and water, excretes more potassium

Question 8

Four steps in the renin-aldosterone-angiotensin pathway

Answer 8

1. Decreased blood volume stimulates renin production from the juxtaglomerular apparatus
2. Renin cleaves angiotensinogen to angiotensin I
3. Angiotensin I is converted to angiotensin II by ACE
4. AT-II is a vasoconstrictor and stimulates release of aldosterone

Question 9

Aldosterone vs AVP

Answer 9

Aldosterone is a primary regulator of the blood volume, whereas AVP is more focused on free water volume

Question 10

Primary high-affinity receptor for aldosterone

Answer 10

MR (nuclear receptor superfamily)

Question 11

To what does the MR bind with high affinity?

Answer 11

Both MCs and GCs

Question 12

Relative concentrations of GCs to MCs

Answer 12

GCs are 100-1000x higher than MCs, but over 95% are bound and aldosterone has no specific binding protein

Question 13

Inactivation of glucocorticoids

Answer 13

Conversion of cortisol to cortisone by 11beta-HSD type 2 in the kidneys

Question 14

Carbenoxolone

Answer 14

Inhibits 11beta-HSD type 2

Question 15

Excessive licorice consumption

Answer 15

Licorice is also a natural inhibitor of 11-beta HSD type 2 and will lead to increased sodium and water retention if eaten too much

Question 16

Adrenal androgen

Answer 16

DHEA(S): dehydroepiandosterone (sulfate)

Question 17

What does DHEA get converted into?

Answer 17

Testosterone and estrogen

Question 18

How many of total androgens come from the adrenal cortex in the prostate?

Answer 18

50%

Question 19

When does androgen peak?

Answer 19

Between 20-30 years old

Question 20

“Weak” androgens

Answer 20

DHEA: low affinity for androgen receptor

Question 21

Pregnenolone

Answer 21

First compound in the synthesis of androgens; converted from cholesterol in the mitochondria

Question 22

Cholesterol ester hydrolyase

Answer 22

Converts cholesterol ester to free cholesterol; enzyme is stimulated by ACTH

Question 23

Rate-limiting step in steroid hormone biosynthesis

Answer 23

StAR protein moving cholesterol from the outer to the inner mitochondrial membrane; regulated by ACTH

Question 24

Desmolase/P450scc

Answer 24

Converts cholesterol to pregnenolone

Question 25

21-alpha-hydroxylase deficiency - hormone levels

Answer 25

Causes excess DHEA, no glucocorticoids, no mineralocorticoids

Question 26

21-alpha-hydroxylase deficiency - clinical manifestations

Answer 26

Masculinization, ambiguous genitalia at birth, sodium loss

Question 27

11-beta hydroxylase deficiency - hormone levels/gene involvement

Answer 27

CYP11B1 deficiency. Excess DHEA, no cortisol

Question 28

11-beta hydroxylase deficiency - clinical manifestations

Answer 28

Salt and water retention due to excess MR activity | Low aldosterone due to low renin, high ANP

Question 29

17-alpha hydroxylase deficiency - hormone levels

Answer 29

No adrenal androgens, decreased glucocorticoids, excess MCs

Question 30

17-alpha hydroxylase deficiency - clinical manifestations

Answer 30

Feminization, sodium and water retention due to excess MR activity

Question 31

What will all the adrenal enzyme deficiencies result in?

Answer 31

High ACTH levels due to lack of feedback

Question 32

CYP11B2 stimulation

Answer 32

Stimulated by angiotensin II, not ACTH

Question 33

Innervation of the adrenal medulla

Answer 33

Splanchnic nerve

Question 34

Cellular architecture of the adrenal medulla

Answer 34

Cords of polyhedral epithelial cells

Question 35

What is epinephrine released in response to?

Answer 35

Acute stress (pain, cold, perceived danger)

Question 36

Speed of movement of epinephrine

Answer 36

Rapid release, rapid return

Question 37

Locations of catecholamine synthesis

Answer 37

Dopamine can be converted to norepinephrine in the peripheral nerves, but epinephrine is ONLY made in the adrenal medulla

Question 38

What stimulates conversion of NE to epi?

Answer 38

Cortisol

Question 39

Through what types of receptors does epi act?

Answer 39

Both alpha and beta adrenergic receptors

Question 40

Arousal effects of epi

Answer 40

Pupil dilation, sweating, GI and bronchial relaxation

Question 41

Metabolic effects of epi

Answer 41

Increased glucose mobilization, increased BMR

Question 42

Cardiovascular effects of epi

Answer 42

Vasoconstriction, tachycardia

Question 43

Three main targets of epi

Answer 43

Muscle, liver, and fat

Question 44

Half life of catecholamines

Answer 44

Very short: 10-90 seconds

Question 45

Degradation of catecholamines

Answer 45

COMT or MAO

Question 46

Metabolic byproduct of catecholamine breakdown

Answer 46

Vanillymandelic acid (VMA)

Question 47

What is the clinical significance of VMA?

Answer 47

Has a longer half-life; can be used to detect tumors secreting NE or epi

Question 48

Pheochromocytomas

Answer 48

Tumors in the chromaffin cells

Question 49

Symptoms of pheochromocytomas

Answer 49

Hypertension without response to meds, headaches, tachycardia

Question 50

Diagnosis of pheochromocytomas

Answer 50

Measurements of urinary metanephrines

Question 51

Treatment of pheochromocytomas

Answer 51

Surgery. (Presurgery: alpha/beta blockers)

Question 52

What is the nickname of pheochromocytomas?

Answer 52

The "10% tumor"