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Post Midterm Biochem > Steroid Hormones > Flashcards

Steroid Hormones Flashcards

1
Q

Cholesterol esterase

A

activated by PKA to do CE–>cholesterol

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2
Q

StAR

A

Steroidogenic acute regulatory protein

transports cholesterol to mitochondria to be converted to pregnenolone

Important regulatory step

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3
Q

Desmolase Complex

A

shortens hydrocarbon chain, hydroxylation of the steroid nucleus: cholesterol side chain cleavage enzyme

Rate limiting step of steroid synthesis

Cyto P450 dependent monooxygenase
also requires NADPH and O2

Located in Mitochondria
aka: CYP 11A1, P450 scc

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4
Q

3-ß-hydroxysteroid dehydrogenase

A 
oxidizs and isomerizes pregnenolone
pregnenolone-->progesterone
17-hydroxypergnenolone-->17-hydroxyprogesterone
DHEA-->Androstenedione
Effects:
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5
Q

Z. Glomerulosa

A

produces aldosterone

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6
Q

Z. fasciculata

A

produces cortisol

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7
Q

Z. Reticularis

A

produces DHEA and aldostedione. Testes finish up testosterone synthesis in males and ovaries convert to estrogens in females

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8
Q

CYP 21A2

A

Progesterone–>deoxycorticosterone
17-hydroxyprogesterone–>11-deoxycortisol
21-hydroxylase
Downstream:alosterone, cortisol

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9
Q

CYP11B

A 
at position 11B
deoxycorticosterone-->corticosterone
11-deoxycortisol-->cortisol
mitochondria
11ß-hydroxylase
Downstream: aldosterone, cortisol
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10
Q

CYP11B2

A

at postition 18
Aldosterone synthase, P450c11as
corticosterone–>Aldosterone

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11
Q

CYP19

A

Androxstenedione–>estrone
Testosterone–>Estradiol
(only effects estradiol synthesis)
A, aromatase

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12
Q

CYP17A1

A 
17alpha-hydroxylase (P450c17)
@ 17alpha
pregnenolone-->17hydroxypregnenolone
progesterone-->17-hydroxyprogesterone
effects cortisol, sex hormones
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13
Q

17,20

A 
17-hydroxyprogesterone-->Androstenedione
17-hydroxypergnenolone-->DHEA
11-Deoxycortisol-->Anrdrostenedione
17, 20 lyase
effects sex hormones
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14
Q

Regulation of cortisol

A

ACTH–>cortisol–|ACTH

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15
Q

Cortisol

A

regulated by ACTH from pituitary

dominant glucocorticoid

synthesized from porgesterone in zona fasciculata

stress adaptation

needed for gluconeogenesis esp during prolonged starvation

degrades muscle (counteracts insulin)

affects immune system:
inhibits PLA2–> down arachidonic acid –> down eicosanoids (prostaglandins, thromboxanes and leukotrienes; Inhibits induction of cox-2

transported bound 75% transcortin, 15% albumin

Inflammation–>binding to transortin reduced–>[cortisol] up–>therefore: cortisol activity up

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16
Q

Aldosterone

A

Principal mineral corticoid
raises blood pressure, fluid volume, increase Na+ uptake

stimulated by angiotensin II/III

17
Q

Estrogens

A

Stimulated by FSH and LH (pituitary)

estrogens: control menstrual cycle, development of 2º sex characteristics

Progesterone: secretory phase of uterus and mammary glands, implantation and maturation of fertilized ovum

18
Q

Androgens

A

dehydroepiandrosterone and androstenedione, testosterone

Z. retiularis and fasiculata
weak androgens converted to estradiol in fat cells and testosterone in testes

19
Q

Testosterone

A

LH–>up [cAMP]–>up PKA activity (leydig cells)

Sertoli cells–>dihydrotestosterone (DHT)

stimulates spermatogenesis, 2º sex characteristics, anabolism, masculinization of fetus

20
Q

steroid receptior

A

Located in cytosol or nucleus, hormone binding leads to (homo/hetero)dimerization, binds HRE, acts as enhanser or repressor of gene transcription

21
Q

3-ß hydrosteroid dehydrogenase deficiency

A

No glucocorticoids mineral corticoids, active androgens or estrogens

increased salt in urine

female like genetalia

22
Q

17-α-hydroxylase deficiency

A

no sex hormones or cortisol

increased mineralcorticoids–>up Na+, up fluids, up bp

female-like genetalia

23
Q

21-α-hydroxylase deficiency

A

most common form of CAH (partial and complete)
mineralocorticoids and glucocorticoids absent or deficient
over production of androgens leads to masculinization of external genitalia in females, early virilization in males

24
Q

11-β-hydroxylase deficiency

A

decrease cortisol, corticosterone, aldosterone
increased deoxycorticosterone–>fluid retention–>suppresses renin/angiotensin system (low renin hypertension)
masculinization and virilization

25
Q

Cushing’s syndrome

A

hypercortisolism/hyperfunction of adrenal cortex (usually due to tumor):
[cortisol] up, [ACTH] down
Protein loss and characteristic fat distribution (face, neck truncus)
hirsutism (early pubic hair)

26
Q

Addison’s disease

A

1º adrenal cortical insufficency (usually autoimmune)

aldosterone and cortisol low; ACTH high

FTT, muscle weakeness, fatigue, weight loss, hyperpigmentation, salt craving, hyponatremia, hyperkalemia, hypovolemia, hypotension, abdominal pain, vomiting, constipation

Post Midterm Biochem (16 decks)

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