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unit 6: MCP > Vitamin D and steroids (19) > Flashcards

Vitamin D and steroids (19) Flashcards

1
Q

What is cholesterol the precursor for?

A
  1. glucocorticoids - cortisol
  2. mineralcorticoides - aldosterone
  3. sex hormones - androgens, estrogens, progestins
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2
Q

Where is the receptor for a steroid ?

A

cytoplasm or nucleus

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3
Q

What is the rate limiting step in steroid synthesis?

A

conversion of cholesterol to 21 C pregenolone

-cyt P450SCC or desmolase

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4
Q

Where is p450 SCC located?

A

on the inner mitochondrial membrane

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5
Q

What protein mediates the movement of cholesterol from the outer mito membrane to the inner?

A

StAR

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6
Q

What happens when there is a defect of 3-B-hydroxysteroid dehydrogenase?

A

-build up of pregnenolone
-no synthesis of any steroids:
glucocorticoids
mineralcorticoids
androgens
estrogens
- female like genitalia

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7
Q

What happens if there is a defect in 17-alpha-hydroxylase?

A
  • build up of progesterone
  • no sex hormones or cortisol

-inc production of mineralcorticoids
Na+ fluid retention –> HTN

-female like genitalia

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8
Q

What happens if there is a 21-alpha-hydroxylase deficiency?

A

-no synthesis of: minercorticoids & glucocorticoids

overproduction of androgens:
masculization of external genitalia in females
early virilization in males

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9
Q

What happens in a 11-B hydroxylase defiency?

A

decrease in cortisol, aldosterone, corticosterone
fluid retention
overproduction of androgens

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10
Q

What deficiency is the most common?

A

21-alpha-hydroxylase

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11
Q

Where is cortisol produced?

A

zona fasiculata of the adrenal cortex

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12
Q

Describe the pathway leading to the release of cortisol?

A
  1. CRH by hypothalamus in response to stress
  2. anterior pituitar releases ACTH
  3. cortisol secreted by adrenal cortex
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13
Q

How does ACTH lead to production of cortisol?

A
  1. G protein receptor - inc cAMP, activated PKA
  2. activation of lipase
    - converts cholesterol esters to cholesterol
  3. activation of StAR
    - cholesterol moves to inner mit membrane
  4. cholesterol–> pregnenolone
    - moves to cytosol
  5. pregnenolone –> progesterone
  6. progesterone –> 11 -deoxycortisol
  7. 11-deoxycortisol –> cortisol
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14
Q

Which enzymes catalyze the conversion of progesterone –> 11-deoxycortisol?

A

CYP17, CYP21

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15
Q

Which enzyme catalyzes the B-hydroxylation at C21 of 11-deoxycortisol to convert it to cortisol?

A

CYP11B1

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16
Q

Where is aldosterone produced?

A

outer layer of the adrenal cortex: zona glomerulosa

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17
Q

What stimulates the production of aldosterone?

A

decrease in plasma Na+/K+

angiotensin II

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18
Q

What converts angiotensinogen to angiotensin I?

A

Renin secreted by kidneys

19
Q

What converts angio I –> angio II?

A

ACE

20
Q

What are ACE inhibitors used to treat?

A

renin dependent BP

21
Q

What are androgens produced by?

A

inner and middle layers of adrenal cortex

zona reticularis

22
Q

What stimulates the release of LH and FSH from the anterior pituitary?

A

GRH from the hypothalamus

23
Q

What is the function of LH?

A

causes testes to produce testoerone, ovaries to produce estrogen and progesterone

24
Q

What is the function of FSH?

A

regulates growth of ovarian follicles

regulates spermatogenesis

25
Q

What enzyme catalyzes the conversion of androstenedione to estrogen?

A

aromatase

26
Q

What are aromatase inhibitors used to treat?

A

hormone (+) breast cancer

27
Q

What motif does the hormone response element associate with in the DNA?

A

zinc finger

28
Q

Where are steroid hormones converted into inactive excretion products?

A

in the liver

29
Q

How does the liver make the steroid hormones water soluble?

A

conjugation with glucoronic acid or sulfate

30
Q

What are the sources of vit D?

A
  1. endogenous - 7-dehydrocholesterol
  2. exogenous:
    ergocalciferol - D2 - plants
    cholecalciferol -D3 - animals
31
Q

What is 7-dehydrocholesterol converted to and where?

A

cholecalciferol in dermis and epidermis with sun

-transported to liver with binding protein

32
Q

What form of vit D is measured by clinical labs to see if someone is deficient?

A

25-OH-D3 or calcidiol

-major form in the plasma

33
Q

What are the two steps that activate cholecalciferol? Name the enzymes, products, and locations

A
  1. Liver:
    enzyme: 25 hydroxylase
    product: 25-OH-D3 (calcidiol)
  2. Kidney
    enzyme: 25-hydroxycholecaliferol 1 hydroxylase
    product: 1,25-diOH-D3 (calcitriol)
34
Q

Is 25-hydroxycholecaliferol 1 hydroxylase mediated directly or indirectly by phosphorous and calcium?

A

Phosphorous - directly
-low P stimulates enzyme

calcium - indirectly
- low ca2+ causes PTH which stimulates enzyme

35
Q

What does the vitamin D receptor form a heterodimer with in the nucleus?

A

RXR - retinoid x receptor

36
Q

What proteins are upregulated in response to RXR-VDR binding to the VDRE?

A

calbindin - allows transport of ca2+ across enterocyte

TRPV5 - entry of ca2+ apically

37
Q

Low plasma calcium has what effects?

A

inc ca2+ absorption and bone resorption

demineralization

38
Q

High plasma calcium has what effects?

A

inhibits bone resorption, inc excretion
mineralization

conversion of 25-OH-D3 to 24,25-DiOH-D3

inc expression of calcitonin

39
Q

What level is considered vit D deficient?

A

<30

40
Q

Above What level of vit D , is considered to have adverse effects?

A

> 125

41
Q

What level is considered adequate vit D?

A

50-125

42
Q

What two diseases does demineralization cause in kids and adults?

A

rickets in kids and osteomalacia in adults

43
Q

What is renal osteodystrophy?

A

chronic kidney disease

dec vitamin D , inc retention of P

44
Q

What does hyperthyroidism cause?

A

lack of PTH

hypocalcemia and hyperphosphatemia

unit 6: MCP (17 decks)

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