Endo 1

Question 1

Cholesterol Synthesis to pregnenolone

Answer 1

Requires cholesterol desmolase being activated by ACTH

-Key rate limiting step

Question 2

Cholesterol Synthesis to pregnenolone

Answer 2

Requires cholesterol desmolase being activated by ACTH

-Key rate limiting step

Question 3

How do I get to Corticosterone from pregnenolone

Answer 3

3 B hydroxysteroid dehydraogenase
21 B hydroxylase
11 B hydroxylase

• if any of these are deficient, will shunt to Cortisol and sex steroids

Question 4

How do I get from pregnenolone to cortisol

Answer 4

17 a hydroxylase,
21 B hydroxylase
11 B hydroxylase

Question 5

If I am deficient in 17 a hydroxylase, what happens?

Answer 5

Shunt to aldosterone

Question 6

If I am deficient in 17 a hydroxylase, what happens?

Answer 6

Shunt to aldosterone

Question 7

If im deficient in 21 B hydroxylase what happens

Answer 7

Shunt to sex steroids only

Question 8

11 B hydroxylase deficiency, what happens

Answer 8

Shunt to sex steroids only

Question 9

If im deficient in 17 20 lyase, what happens

Answer 9

Shunt to cortisol and aldosterone

Question 10

How do I get from corticosterone to aldosterone (last step in forming aldosterone)?

Answer 10

Aldosterone synthase is stimulated by angiotensin II (RAS)

Question 11

From superficial to deep, what is the adrenal gland cortex

Answer 11

Aldosterone top - G glomerulosa
Cortisol middle - F fasiculata
DHEA bottom - R reticularis

Question 12

ACTH stimulates ultimately what hormones to be released

Answer 12

All of them in the adrenal cortex

Question 13

When aldosterone is created in the cortex, what does it do

Answer 13

Travel through the blood to the distal tubules of the kidney to cause transcription of sodium transport channels.

Inserts sodium channels in DCT.

Then it excretes K to retain Na and increase volume/blood pressure

Question 14

What stimulates the RAAS system

Answer 14

Low renal perfusion from low blood volume.

Hyperkalemia.

Question 15

How does aldosterone negative feedback work?

Answer 15

Increased blood volume
Increased BP
Increased sodium
Or low potassium

Then

Negative feedback on CRH
Decreased released of ACTH
Decreased release of aldosterone

Question 16

Where are androgens produced

Answer 16

DHEA, DHEAS, and androstenedione (not corticosterone)

In the cortex in both genders. Produced mostly by the zonal reticularis. Some produced by zonal fasciculate

produced in the gonads. Produced by gonads in males and adrenal cortex in both M and F

Question 17

DHEA and DHEAS function

Answer 17

Less potent.
Secondary sex characteristics in adolescence and childhood

Question 18

What does a deficiency in 17 ketosteroid reductase cause

Answer 18

Absence of testosterone

Question 19

Precursor to both estrogen and testosterone

Answer 19

Androstenedione

Question 20

During puberty you get pulsatile release of what

Answer 20

CRH, which gives you an abundance of ACTH to get secondary sex characteristics

Question 21

In general how is CRH released outside of certain periods in puberty

Answer 21

Pulsatile on a day to day basis.
Pulses before waking. - help to wake up
In response to stressors. - need stress to fight the bear.

Question 22

What does glucocorticosteriod mean

Answer 22

Gluco means sugar, cortico means steroid.

Function is to mobilize sugar.

Cortisol is a glucocorticosteriod

Question 23

What does mineralcorticosteriod mean

Answer 23

Mineral means things like potassium

Cortico means steriod.

Example is aldosterone

Question 24

What does cortisol bind to and its effect on hormones

Answer 24

It binds to glucocorticosteroid receptor with high affinity

It binds to mineralcorticosteroid receptor with low affinity.

When concentration is high enough it will have same effect on kidney as aldosterone.

Question 25

Cortisol actions on the body

Answer 25

Gluconeogensis; protein metabolism and dec protein synthesis. Also break down fat for same thing. Mobilize aa to liver for gluconeogenesis
- mobilizing energy

Anti insulin. Cause insulin insensitivity

Anti inflammatory by inhibit release of histamine and serotonin from mast cells. Incr synthesis of A2 inhibitor. Inhibit syn of IL2. Inhibit prod. Of T lymphocytes. Inhib precursor of prostaglandin.

IL 2 is a cytokine, serotonin causes vasodilation. Prostaglandin increases pain and fever. So want to inhibit these

Increase vascular response to catecholamines. Upregulates a1 receptors on arterioles whicj incr. sens to NE. ; excess of cortisol causes incr arterial pressure

Question 26

Why does adrenal hypertrophy happen with high ACTH (chronically)

Answer 26

Overtime, ACTH up-regulates its own receptor. It does this to increase sensitivity of ACTH

For example its like having a tumor that continuously pumps out cortisol regardless of negative feedback

Question 27

Why does dexamethasone suppression test work

Answer 27

When you give a low dose of dexamethasone to a patient before bed, their ACTH hypertrophy or tumor should act independently if the negative feedback

Question 28

What should happen normally after a dexamethasone suppression test

Answer 28

They should wake up with low ACTH, low CRH because CRH is inhibited by negative feedback. Only if the negative feedback is working.

If not working, ACTH and CRH would keep pumping independent of the negative feedback loop

Depends if you give a high or low dose of dexa though and the underlying path if its a tumor of the adrenal cortex or ACTH secreting tumor

Question 29

ARE catecholamines UNDER CONTROL by the HPA axis?

Answer 29

No,
Act independently of it

Question 30

What are catecholamines released by

Answer 30

Cheomaffin cells which synthesize cat crom amino acid tyrosine
1:4 ratio of NE to Epi