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Biochemistry Test 3 > Steroid Hormone Metabolism 2 > Flashcards

Steroid Hormone Metabolism 2 Flashcards

1
Q

What is the second messenger that stimulates the synthesis and secretion of cortisol?

A

cAMP

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2
Q

What is the second messenger that stimulates the synthesis and secretion of aldosterone?

A

Phosphotidylinositol cascade - IP3 and DAG

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3
Q

Name the second messenger that is produced as a result of atrial natriuretic factor binding to kidney cells.

A

cGMP is the second messenger produced as a result of ANF binding to kidney

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4
Q

Guanylate cyclase catalyzes the formation of _____

A

cGMP

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5
Q

Cholesterol esterase catalyzes the formation of ___________.

A

cholesterol ( from cholesterol-ester)

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6
Q

The hormone that triggers synthesis and secretion of adrenal steroids is _____.

A

ACTH

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7
Q

Desmolase (20,22-lyase) catalyzes the formation of ___________.

A

Pregnenolone (from cholesterol)

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8
Q

CYP is defined as _________.

A

Genes that encode for P450 hydroxylase enzymes.

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9
Q

The conversion of angiotensin I to angiotensin II is catalyzed by _________ ___________ _________.

A

Angiotensin converting enzvme (ACE)

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10
Q

In congenital adrenal hyperplasia, the enzyme that is deficient is

A

CYP21A2 (cytochrome P450 steroid 21-hydroxylase)

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11
Q

Adrenal insufficiency causes __________ disease.

A

Addison’s

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12
Q

Name 2 reasons for Cushing’s syndrome.

A

Prolonged exposure to glucocorticoids caused by usage of cortisol or tumors of adrenal cortex (It results in elevated blood glucose)

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13
Q

Name an adrenal steroid that causes hypertension upon its overproduction.

A

Mineralocorticoids, such as aldosterone, can cause hypertension upon excessive secretion due to adrenal tumor.

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14
Q

Name an aldosterone antagonist

A

Spironolactone

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15
Q

Name 3 competitive inhibitors of ACE.

A

Captopril, Lisinopril and enalapril

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16
Q

Pregnancy is maintained by continuous secretion of progesterone, which is stimulated by the hormone ___.

A

LH (leutinizing hormone)

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17
Q

Describe how apoptosis is stimulated during the ovarian cycle.

A

Apoptosis is stimulated during ovarian cycle by the removal of the steroids estradiol and progesterone. Apoptosis is a suicide process in which all degradative enzymes (proteases, nucleases, and lipases) are stimulated to cause destruction of the cell.

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18
Q

Testosterone to estradiol conversion is catalyzed by ____________

A

Aromatase

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19
Q

Two hormones that stimulate luteolysis are ________ and _________.

A

Oxytocin and PGF2a

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20
Q

Human placenta lacks the hydroxylase enzyme _____ .

A

CYP17 (this enzyme synthesizes estrogen from DHEA)

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21
Q

Testicular feminization is the result of deficiency of ___________________.

A

5-alpha-reductase (this enzyme reduces Testosterone to the more potent DHT)

22
Q

Cortisol is transported form site of synthesis (adrenal gland) to the target tissue by __________.

A

transcortin

23
Q

Transcortin binds to _________________.

A

the target tissue of cortisol (liver, muscle, adipose tissue)

24
Q

Testosterone is transported by _____________________________________.

A

Testosterone-estrogen-binding protein (TEBP) - all androgens and estrogens

25
Q

A plasma protein that binds nonspecifically to steroids is ________.

A

albumin

26
Q

Name 2 compounds that inactivate steroids upon conjugation.

A

Steroids are inactivated in liver by conjugation with glucouronides or sulfates, which are then excreted in urine. UDPG for glucouronidation and PAPS for sulfonation.

27
Q

Receptors for FSH, LH, GnRH, Angiotensin II and III are located on the ________ __________.

A

Plasma membrane

28
Q

Receptors for cortisol and aldosterone are located in the __________.

A

Cell interior (cvtosol)

29
Q

Receptors for testosterone, estrogen and progesterone are located in the _______.

A

Nucleus

30
Q

What are heat shock proteins?

A

Heat shock proteins are cytosolic proteins that occlude the DNA binding region of the cortisol and aldosterone receptors and cause the receptors to be inactive. Upon binding of the steroid to the receptor the hsp dissociates, and the receptor assumes an active conformation, where it can enter the nucleus and bind DNA and activate transcription.

31
Q

Define hormone response element.

A

Hormone response element is a region of DNA to which a hormone receptor complex can bind to and activate transcription.

32
Q

Glucocorticoids cause the repression of ___________________ _____ .

A

Proopiomelanocortin gene (POMC)

33
Q

The active conformation of the steroid hormone receptor is a dimmer (T/F).

A

False - It is a trimer

34
Q

Describe the DNA binding domain of hormone receptor.

A

The DNA binding domain of hormone receptors shares 60-95% homology between steroid receptor classes. They also contain Zn fingers.

35
Q

What are Zn fingers?

A

Zn fingers are secondary structures that are formed in the DNA binding domain that facilitate binding to DNA near the transcription initiation complex.

36
Q

What are the secretion signals for aldosterone, cortisol, testosterone, 17-beta-estradiol and progesterone respectively?

A

1) Aldosterone - hypovolemia and decreased Na+ concentrations.
2) Cortisol - low Na +
3) Testosterone - LH acting on the Leydig cells.
4) 17-beta-estradiol - a cAMP second messenger system, pregnancy.
5) Progesterone - the embryo (LH and human chorionic gonadotropin), pregnancy

37
Q

Name the bone forming and bone resorbing cells. Name some bone antiresorptive compounds.

A

1) Bone Forming - osteoblasts
2) Bone resorbing - osteoclasts
3) Antiresorptive compounds - Bisphosphanates, Alendronate (Fosamax), and Risedronate (Actonel)

38
Q

Name a catabolic product of estradiol the induces breast cancer.

A

16-hydroxy estrogen (16-OHEN) a side effect of Hormone Replacement Therapy for osteoporosis.

39
Q

What are the compounds that are being used in hormone replacement therapy (HRT) treatment (for postmenopausal women)?

A

Equine estrogen/medroxy progesterone (progestin)

40
Q

Name the universal sulfonate donor compound.

A

3’-phosphoadenosine 5’-phosphosulfate (PAPS).

41
Q

What happens if there is a deficiency in adrenal isoform of desmolase activity? Describe the clinical problems associated with this condition.

A

Deficiency is desmolase leads to inability to produce pregnenolone (steroid precursor). If only the adrenal isoform is affected then the person will have Addison’s disease which is an OVERALL deficiency of adrenal steroid hormones (aldosterone and cortisol lacking). Causes high ACTH, hypoglycemia, and low bloodpressure.

42
Q

Describe the biochemical basis of Congenital adrenal hyperplasia.

A

A genetic defect that results in insufficient cortisol production. This causes very high levels of ACTH (not feedback-inhibited), Progesterone accumulates creating DHEA and androsteinedione, causes virilization in females, precocious sex organ development in prepubertal males, and disease related to salt imbalance due to decreased levels of aldosterone.

43
Q

Describe the biochemical basis of Addison’s disease.

A

Overall dificiency of adrenal steroid hormones. ACTH levels are high, hypoglycemic patient (due to low cortisol levels), low blood pressure due to low levels of mineralocorticoids.

44
Q

Describe the biochemical basis of Cushing’s Syndrome.

A

Prolonged exposure to glucocorticoid (Due to the usage of cortisol as an anti-inflammatory drug or due to tumors of adrenal cortex) results in high blood glucose. Patients have truncal obesity but have thin arms and legs and may have hypertension.

45
Q

Describe the biochemical basis of hypertension.

A

Excessive secretion of mineralocorticoids resulting from adrenal tumor. Treated with aldosterone antagonists (spironolactone) or competitive inhibitors of ACT (captopril, Lisinopril, and enalapril).

46
Q

Describe the biochemical basis of osteoporosis.

A

Estrogens induce the synthesis of osteoprotegrin, which causes osteoblast differentiation, and suppress osteoclasts. Lack of estrogens can lead to reduction in bone mass, especially in post-menopausal women.

47
Q

Describe the biochemical basis of testicular feminization.

A

Genetic deficiency in 5-alpha-reductase, which causes a reduction in DHT (an androgen that promotes the differentiation of male sexual characteristics. XY with female gentalia (phenotypically, but do not actually have ovaries or uterus).

48
Q

Describe the role of fetal adrenal and fetal liver with reference steroid metabolism during pregnancy.

A

Human placenta lacks CP17 (needed to make DHEA which is precursor to Estrogen). The Fetal adrenal gland converts cholesterol to DHEA, then is transported to the fetal liver forming 16-alpha-hydroxy-DHEA. Aromatization will result in 17-Beta-estradiol.

49
Q

Describe the process of estradiol mediated programmed cell death.

A

A drop in estradiol and progesterone will result in the sloughing of the endometrium (menstration). Degradative enzymes (proteases, nucleases, and lipases) are stimulated to cause cell death. Leads to menstruation.

50
Q

Describe atrial natriuretic factor (ANF) mediated signaling.

A

ANF comes from heart atrial cells that oppose the actions of angiotensin. Binds to Zona glomerulosa cell receptors which activates guanylate cyclase leading to the formation of second messenger cGMP from GTP. cGMP antagonizes aldosterone synthesis and secretion

51
Q

Describe the key enzymes of the steroid metabolism (generic names).

A

Cholesteryl esterase (cholesterol-ester to cholesterol), Desmolase (cholesterol to pregnenolone), Cytochrome P450 hydroxylase enzymes (17-hydroxylase, 21-hydroxylase, etc) (pregnenolone to progesterone and progesterone to cortisol and aldosterone).

52
Q

Describe the mechanism of P-450 hydroxylase catalyzed reaction.

A

P-450 hydroxylases use molecular oxygen as a substrate, where only one oxygen atom is incorporated into the steroidal substrate (as OH) and the second atom reduced to water molecule. (Electrons are donated by NADPH)

Biochemistry Test 3 (10 decks)

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