2. Adrenals

Front 1

The 2 componenets of the adrenal gland are:

Back 1

1. Medulla
2. Cortex

Front 2

What does ea component produce?

Back 2

Medulla: epi/norepi/dopamine
Cortex: androgens, glucocorticoids, mineralcorticoids.

Front 3

What are epi/norepi/dopamine known as collectively?

Back 3

Catecholamines

Front 4

What causes the release of catecholamines?

Back 4

Sympathetic fibers firing in the adrenal medulla.

Front 5

What causes the sympathetic fibers to fire and stimulate catecholamines?

Back 5

Stress, exercise, hypoglycemia, and trauma.

Front 6

How are catecholamines carried through the body?

Back 6

Bound to albumin and serum proteins.

Front 7

What are the targets of catecholamines?

Back 7

Alpha/Beta adrenergic receptors

Front 8

Which catecholamine acts on the heart, and how?

Back 8

Epinephrine - increases HR and contraction force by acting on beta-adrenergic receptors.

Front 9

Which catecholamine acts on blood vessels and how?

Back 9

Norepinephrine - constricts BV's and increases resistence and arterial BP.

Front 10

What other things do epi and norepinephrine do?

Back 10

-Dilate bronchioles
-Stimulate lipolysis
-Increase metabolic rate
-Promote glycogenolysis
-Dilte pupils, inhibit gastrointestinal digestion.

Front 11

What is the most common pathology of the adrenal medulla?

Back 11

Pheochromocytoma - a benign adenoma in its chromaffin cells

Front 12

What is the #1 neoplasm in kids?

Back 12

Neuroblastoma

Front 13

what's a pheochromocytoma often called?

Back 13

the 10% tumor

Front 14

What methods are used for detecting pheochromocytoma? (4)

Back 14

1. Plasma catecholamines
2. Urine catecholamines
3. Urine metanephrines
4. Urine VMA

Front 15

what is VMA?

Back 15

Vanillylmandelic acid; the degradation product of norepi and epinephrine.

Front 16

What is the degradation product of dopamine?

Back 16

HMA - homovanilic acid

Front 17

what is another degradation product of epinephrine?

Back 17

metanephrine (MN)

Front 18

what is another degradation product of norepinephrine?

Back 18

normetanephrine (NMN)

Front 19

what is the more sensitive test for pheochromocytoma?

Back 19

24-hour urine catecholamines and metabolites.

Front 20

What are some tips to remember re: catecholamine specimens?

Back 20

-May need >1 24hr urine collecn
-Measure creatinine to ensure that it's a 24 hr urine.
-Don't add a preservative
-Use plasma for better sensitivity than serum

Front 21

The catecholamines are amino acid hormones; what is a similar molecule that's more of a neurotransmitter?

Back 21

SEROTONIN

Front 22

what is serotonin?

Back 22

a monoamine neurotransmitter

Front 23

what's another name for serotonin?

Back 23

5-HT; 5-hydroxytryptamine

Front 24

Where is serotonin made?

Back 24

-CNS: In serotonergic neurons
-Intestine: enterochromaffin cells

Front 25

what are some important fucntions of serotonin?

Back 25

-Sleep regulation
-Smooth muscle releaxation
-Cardiovascular function
-GI/vascular contraction

Front 26

what type of tumor is most often related to serotonin?

Back 26

Carcinoid tumor - of the small bowel.

Front 27

What is 5-HIAA?

Back 27

a degradation product of serotonin; measuring both of these in urine will indicate carcinoid tumors.

Front 28

What is the adrenal cortex a factory for?

Back 28

steroids!!
(corticosteroids that is)

Front 29

The 4 steroids we're mainly focused on:

Back 29

1. Estrogens
2. Testosterone
3. Cortisol
4. Aldosterone

Front 30

what are the corticosteroids synthesized from?

Back 30

Cholesterol!

Front 31

What does aldosterone do?

Back 31

Acts on kidney distal tubule; increases Na uptake, K excretion. Increases water resorption

Front 32

What is the ultimate consequence of aldosterone?

Back 32

Increased extracellular fluid.

Front 33

What does cortisol do?

Back 33

Increases and maintains normal blood glucose levels.

Front 34

How does cortisol work?

Back 34

-Mobilizes amino acids/fat
-Stimulates liver gluconeogenesis.
-Suppresses immune system
-Promotes lung maturation and surfactant production.

Front 35

What do the androgens do?

Back 35

function in sex

Front 36

What regulates the adrenal cortex in general?

Back 36

ACTH

Front 37

But what feedback regulates aldosterone?

Back 37

-Increased K
-Decreased Na
-Angiotensin II due to decr renal blood flow
-ACTH is short-term

Front 38

What suppresses aldosterone?

Back 38

-High Na
-Low K
-ANH

Front 39

What is ACTH much more active in controlling?

Back 39

Cortisol

Front 40

What stimulates CHR release?

Back 40

Physical and mental stress

Front 41

What regulates the androgens partially?

Back 41

ACTH

Front 42

What is adrenal cortex
-Hypofunction?
-Hyperfunction?

Back 42

Hypo = Addison's disease

Hyper = Cushing's disease

Front 43

How would you differentiate between Primary adrenal insufficiency and ACTH-dependent?

Back 43

ACTH primarily controls cortisol, so aldosterone would be less decreased; also ACTH would be decreased in the latter.

Front 44

What are the diagnostic levels of Cortisol and ACTH for diagnosing hypofunction?

Back 44

Cortisol: <10 ug/dL
ACTH: >250 pg/mL

Front 45

and quickly, corticosteroid excess IS?

Back 45

CUSHINGS

Front 46

MOST COMMON CAUSE OF CUSHINGS:

Back 46

exogenous glucocorticoid treatment

Front 47

Screening tests for hyperadrenalism:

Back 47

-Serum/urine free cortisol
-ACTH levels

Front 48

How would you know if Cushing's disease was ACTH independent?

Back 48

-ACTH levels would not be high
-Overnight dexamethasone suppression would not change with high dose.

Front 49

So what is the confirmatory test for cushing's?

Back 49

Overnight dexamethasone suppression with high dose will show change because the ACTH is so high it STILL stimulates production.

Front 50

How does an adrenal tumor affect cortisol, ACTH, and CRH levels?

Back 50

-Cortisol is increased
-ACTH is decreased
-CRH is decreased

Front 51

What is mineralcorticoid excess?

Back 51

Aldosteronism

Front 52

What is the name for primary mineralcorticoid excess?

Back 52

Conn's syndrome

Front 53

How is Conn's syndrome diagnosed?

Back 53

By measuring renin and aldosterone levels.

Front 54

List 5 assays for assessing adrenal function:

Back 54

1. Cortisol (blood and urine)
2. Aldosterone
3. 11-deoxycortisol
4. 17-hydroxyprogesterone
5. PRA - plasma renin activity

Front 55

What is 17-hydroxyprogesterone?

Back 55

the precursor to cortisol

Front 56

what is 17-hydroxypregnanolone?

Back 56

the precursor to testosterone

Front 57

what is progesterone?

Back 57

the precursor to aldosterone.

Front 58

How is a low-dose Dexamethosone test done?

Back 58

1. Draw baseline blood cortisol
2. Give 1 mg Dexameth at 11pm
3. Draw blood at 8am

Front 59

What are the results of lo-dose dexamethosone testing in:
-normal individuals?
-Cushing's syndrome?

Back 59

Normal: <3ug/dl serum, <100ug/dl in urine.
CS: >10ug/dl serum, >120 ug/dl in urine.

Front 60

What is high-dose dexamth suppression useful for?

Back 60

Differentiating Primary Cushing's (suppression occurs) from 2dary (ACTH stimulated) where no suppression occurs.

Front 61

RECAP: for cushing's syndrome,
-What are screening tests?
-What are confirmatory tests?

Back 61

Screens: Urine cortisol and lo-dose DM test.

Confirm: Plasma ACTH, serum cortisol, hi-dose DM test.

Front 62

What's the principle of the metapyrone stimulation test?

Back 62

Inhibiting 11-hydroxylase blocks cortisol synthesis (metapyrone inhibits the enzyme)

Front 63

What metapyrone stimulation results are seen in:
-healthy patients?
-Cushing's?

Back 63

Healthy: cortisol levels drop
Cushing's: ACTH increases.