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COM - Endocrine > Steroid Biosynthesis - 2/1 Theisen > Flashcards

Steroid Biosynthesis - 2/1 Theisen Flashcards

1
Q

What is responsible for stimulating the production of surfactant in neonates?

Premature babies develop what due to the lack of this hormone?

A

Glucocorticoids

Infant respiratory distress syndrome

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2
Q

Cortisol is converted to cortisone with what enzyme?

What can inhibit this enzyme?

Causing what?

A

11-Beta-hydroxysteroid dehydrogenase

Licorice bc it has isoflavones

Hypertension due to salt retention

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3
Q

What enzyme converts testosterone to DHT?

What can inhibit this enzyme

What is the inhibitor used to treat?

A

5alpha-Reductase

Finasteride

Baldness, benign prostatic hyperplasia

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4
Q

What hydrophobic molecules can cross the CM and get into the cytoplasm?

A

O2, CO2, N2

Steroid hormones

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5
Q

Where are steroid hormones synthesized from cholesterol in the body?

Where do these tissues get cholesterol from?

A

SER of adrenal cortex, ovaries, testes

Circulating LDL, de novo from acetyl CoA or cholesterol esters

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6
Q

What is the 1st step in steroid hormone synthesis?

What enzyme is used?

How is the starting product modified?

A

Cholesterol -> pregnenolone

Desmolase (RLS)

Adds a C=O and cleaves 6C off side chain

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7
Q

What stimulates the conversion of cholesterol to pregnenolone?

A

ACTH

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8
Q

The conversion of pregnenolone to progesterone requires what enzyme?

A

3-Beta-hydroxysteroid dehydrogenase

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9
Q

The conversion of pregnenolone to 17-alpha-Hydroxypregnenolone requires what enzyme?

A

17-alpha-hydroxylase

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10
Q

Progesterone is converted into aldosterone where?

Cortisol where?

Estradiol where?

Testosterone where?

A

Adrenal cortex ZG

Adrenal cortex ZF

From testosterone in ovaries

From DHT in testes

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11
Q

Where is desmolase found?

What family is it from?

A

Gonads and adrenal cortex

P-450, monoxide base

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12
Q

When is ACTH secreted?

From where?

What does it stimulate?

A

Stressful conditions (hypoglycemia, cold, exercise)

From pituitary gland

Release of cortisol from adrenals

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13
Q

What else will increase the activity of desmolase?

A

LH

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14
Q

What stimulates estradiol production in the ovaries?

What enzyme does this activate?

A

FSH

Aromatase

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15
Q

What inhibits the production of GnRH from the hypothalamus?

A

Progesterone

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16
Q

In males what inhibits FSH?

LH?

A

Inhibin

Testosterone

17
Q

In females, what inhibits the production of FSH and LH from the pituitary gland?

A

Progesterone

Estradiol (early-mid follicular phase)

18
Q

In females what stimulates the formation of FSH and LH from the pituitary gland?

A

Estradiol (late follicular phase)

19
Q

What does FSH and LH make in the ovaries?

A

Estradiol

Progesterone

20
Q

A defect in what enzyme will cause deficiencies in mineral and glucocorticoids?

A

21-hydroxylase

21
Q

21-hydroxylase defects leads to what?

Specifically what in females?

A

Hyponatremia, hypotension, hypoglycemia

Virilism due to INC flow of intermediates into adrenal androgens

22
Q

Deficiency in 17-a-hydroxylase causes what?

A

Loss of cortisol and sex steroids

Dec in cortisol is compensated by corticosterone

23
Q

Defects in 11-B-hydroxylase cause what?

A

Hypertension due to accumulation of 11-deoxycorticosterone

24
Q

Aldosterone is made from what? Where?

Excessive levels Cause what?

A

Progesterone, in adrenal cortex (zona glomerulosa)

Conn syndrome - INC BP, HTN, hypernatremia

25
Q

What is Cushing syndrome caused by?

Characteristics?

A

Too much cortisol

Excess fat on face and trunk

26
Q

How are glucocorticoids and progesterone transported in the blood?

Testosterone, DHT, estradiol carried by what?

Where are these carrier proteins made?

A

CBG

SHBG

Liver

27
Q

What are the effects of ADH?

A

Vasoconstriction, stimulates thirst, INC water retention

28
Q

What causes immunosuppression by inhibiting cellular and humoral responses?

How?

A

Glucocorticoids and cortisol

Induce I-Kba which sequesters NF-KB in its inactive form in the cytoplasm

29
Q

What else can cortisol cause via immene suppression?

A

T-cell apoptosis

30
Q

Too little Vitamin D causes what?

Too much?

A

Rickets, osteomalacia, hypocalcemic tetany

Hypercalcemia/calciuria -> dazed appearance, no appetite, sarcoidosis (granulomas in skin, lungs, LNs)

31
Q

What is the active form of Vit D?

A

Calcitriol (1,25-dihydroxycholecalciferol)

32
Q

Is Vit D classified as a steroid?

How does it act?

A

NO

Binding to nuclear receptors and altering the expression of target gene containing VDRE

33
Q

What enzyme helps to form active Vit D after UV exposure to the skin?

A

7-dehydrocholesterol

34
Q

In intestinal cells what does Vit D come from?

A

Ergocalciferol (Vit D2)

35
Q

What enzyme in the liver is needed in Vit D synthesis?

Kidney?

A

25-hydorxylase

1-alpha-hydroxylase

36
Q

1-alpha-hydroxylase can be activated by what?

inactivated by what?

A

PTH, low PO4

Calcitriol

37
Q

What does Calcitriol increase?

What does it stimulate?

Inhibit?

A

Ca reabsorption from intestine, kidneys, and bone

PTH

Calcitonin

38
Q

What is responsible for regulating VG Ca2+ channels on sperm, prepares the uterus for implantation, causes smooth m. Relaxation and DEC mother’s immune response?

Dec in this hormone precedes what?

A

Progesterone

Menstruation, labor, lactation

COM - Endocrine (12 decks)

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