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GIGU Exam 2 > Sterioid Biosynthesis > Flashcards

Sterioid Biosynthesis Flashcards

1
Q

Desmolase

A

An enzyme that produces pregnenolone from cholesterol

adds =O to cholesterol

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2
Q

All steroids are made from what and where

A

Cholesterol in the Adrenal cortex

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3
Q

What regulates Desmolase Activity

A

ACTH

Stimulates production of pregnenolone from cholesterol

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4
Q

What is Pregnenolone made into

A

Progesterone——>

  1. Corticosteroids (Aldosterone-glucocorticoid + Cortisol-mineralcorticoid)
  2. Sex Hormones (Testosterone + Estradiol)
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5
Q

20,22- Desmolase (cytochrome P450 or CYP11A1)

Action and regulation and where

A

Catalyze RLS to convert cholesterol to Pregnenolone or other things
In Adrenal glands, testes, ovaries, placenta)
Regulated by ACTH

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6
Q

CYPS in animals

Maybe you have to know

A

CYP1-49 and CYP3001-4999

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7
Q

C21

A

Pregnenolone

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8
Q

Aldosterone direct function

A

Binds to Mineralcorticoid Receptors (MR) to activate it

= causing sodium retention and HTN

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9
Q

MR classification

A

Important Nuclear Receptor Superfamily Member (receptor in nucleus so lipophilic ligands bind to it)

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10
Q

5 Hs. That bind to MR

A 
Aldosterone 
11-deoxycorticosterone
Testosterone 
Cortisol (Hydrocotisone)
Cortisone
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11
Q

Primary Aldosteronism

A

CONN’S SYNDROME

Excessive Aldosterone from AC- HTN (Na+ retention and K+ loss)

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12
Q

Adrenal Hyperplasia

A

Mild form is common (not rate as thought)- not easily Dx
1. Classic
2. Non- Classic
= deficiency in adrenal enzymes used to make glucocorticoids
= increase in cortisol and androgen production

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13
Q

Adrenal Hyperplasia Sx:

A

*Hirsutism (in women) = hair on parts of body where excessive hair in not normal
*Oligomenorrhea (in women) = infrequent or very light mentruation (>35days) + infertility at times
Life-threatening sinus/pulmonary infection
Orthostatic syncope
Short
Severe acne

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14
Q

When is adrenal hyperplasia Dx in the fetus

A

Do it while it is in the womb by HLA haplotype

Excessive cortisol in the amniotic fluid

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15
Q

Adrenal Hyperplasia Tx:

A

Monitored H. Replacement Therapy (HRT) = enhance quality of life

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16
Q

2 enzymes that can be mutated in adrenal Hyperplasia

A
  1. 21-Hydroxylase

2. 11-B Hydroxylase

17
Q

X 21- Hydroxylase

A

X Progesterone —> Deoxycorticosterone = ALDOSTERONE
X 17a- Hydroxyprogesterone—> 11-Deoxycortisol = CORTISOL

Increased: progesterone + 17a-Hydroxyprogesterone

18
Q

X 11-B Hydroxylase

A

X Deoxycorticosterone—> Corticosterone = ALDOSTERONE
X 11-Deoxycortisol —> Cortisol = CORTISOL

Increased Deoxycorticosterone + 11-Deoxycortisol

19
Q

Which CYP is 11-B Hydroxylase

And how does it cause HTN

A

CYP11B1
Decrease in cortisol and cortisone (X 11B Hydr.)
Increase in 11-Deoxycorticosterone + 11- Deoxycortisol
* 11-Deoxycorticosterone = BINDS TO MR =HTN

20
Q

The Hypothalamic Pituitary Axis for the release of CORTISOL

A

CRH (hypothalamus)——> ACTH (AP)——> cortisol (Adrenal Glands)——I hypo and AP

21
Q

ACTH binds to what and where in detail

A

ACTH G-protein receptors on the Zona Fasciculata of adrenal cortex

22
Q

ACTH signal cascade when it binds to a receptor

A

ACTH——> ACTHR

  1. Conformational change of G-Protein
  2. Adenylyl cyclase
  3. cAMP
  4. PKA activated and activated cell proliferation to make cortisol and release it
23
Q

ACTH signaling cascade in tumor cell when it binds to R

A

PKA is uncoupled from the G-Protein signal cascade and continuously activated cell proliferation and Cortisol release

24
Q

What is CYP17A1 (17,20 -Lyase)

A 
Dual enzyme (17a-Hydroxylase + 17,20-lyase) 
= MAKES Progestins, mineralocorticoids, glucocorticoids, androgens, estrogens
25
Q

X 17,20-lyase

A

X androgens
INCREASE glucocorticoids (especially CORTISOL =adrenal hyperplasia)
Increase in 17a-hydroxypregnenolone(making DHEA) + 17a-Hydroxyprogesterone(making Androgenedione)
(Mutations in the CYP17A1)
= target for prostate cancer drugs

26
Q

Zona Glomerulosa

A

Aldosterone

27
Q

Zona Reticularis

A

Androgens

28
Q

How is VIT D made

A

7-Dehydrocholesterol + Light = VIT D3———> Calcitetrol eventually

29
Q

How is VIT D3 obtained (Cholecalciferol)

A
  1. DIET : Ergocalciferol (VitD2) in GI
  2. LIGHT: converted from 7-dehydrocholesterol (ON SKIN) ——> 1,25-Dihydroxycholecalciferon
    * BY 1-a- Hydroxylase in kidney
30
Q

Active form of VIT D

And where is it stored

A

Calcitriol
1,25- Dihydroxycholescaliferol
In the liver

31
Q

7-Dehydrocholesterol in skin

Details on how it gets converted to active VIT D

A
  1. UV -> Cholecalciferol (VIT D3)
  2. LIVER -> VIT D3 ——> 25-hydroxycholecalciferol * 25-Hydroxylase
  3. KIDNEY -> 25-Hydroxycholecalciferol ——> 1,25-Dihydroxycholecalciferol
32
Q

Which enzyme does the liver have to convert VIT D3 to a form that it can go to the liver

A

25- Hydroxylase

33
Q
  • and + regulation in kidney to convert 25-HCC to 1,25-DHCC
A
  • Calcitriol (active VIT D)

+ PTH, low PO4-3

34
Q

Enzyme in kidney that makes active VIT D

A

1a- Hydroxylase

35
Q

Which is the protein2 bound form of VIT D

A

25- Hydroxycholecalciferol that is made in the liver

GIGU Exam 2 (13 decks)

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