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Repro Physio > Male Repro Endocrinology > Flashcards

Male Repro Endocrinology Flashcards

1
Q

What does the SRY gene encode? What will it help transform?

A

Testis determining factor (TDF) Indifferent gonad becomes testes, germs cells become spermatogonia

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2
Q

What are characteristics of phenotypic sex?

A

Accessory sex organs develop; external genitalia like penis, scrotum, urethra; secondary sex characteristics

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3
Q

How can you have an XX male? What is this a product of?

A

Translocation of the SRY gene from a Y chromosome to the X chromosome of the father before the sperm fertilizes the ovum; unequal recombination event

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4
Q

How do you get an XY female?

A

If the Y chromosome from the father lacks the TDF

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5
Q

When is the gonad considered indifferent?

A

Before differentiation into testis or ovary

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6
Q

In males, what does the mesonephros become?

A

Epididymis

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7
Q

In males, what does the Wolffian (excretory/mesonephric) duct become?

A

Vas deferens, seminal vesciles, and ejaculatory duct

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8
Q

In males, what happens to the Mullerian/paramesonephric ducts that doesn’t happen to females?

A

In males, they degenerate; in females, they develop into fallopian tubes, uterus, and cervix

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9
Q

What causes Mallerian ducts to degenerate?

A

Anti-Mullerian hormone (AMH) from Sertoli cells

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10
Q

What do androgens made by Leydig cells promote? What does this require?

A

Wolffian duct development and derived structures; Testosterone!!

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11
Q

What does prostate development require?

A

DIHIDROXYTESTOSTERONE

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12
Q

What would lead to development of female structures?

A

LACK OF TESTOSTERONE!!

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13
Q

Besides prostate development, what does DHT regulate?

A

formation of male external genitalia

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14
Q

What word describes GnRH stimulation, and LH and FSH release?

A

Pulsatile!

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15
Q

What can prevent LH and FSH release? What can this method treat?

A

Constant levels of GnRH; treat prostate cancer

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16
Q

What does GnRH bind? What does it trigger?

A

GnRH receptors on gonadotrophs in AP; leads to PLC activation, IP3/DAG, and PKC activation along with IC Ca release

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17
Q

What kind of feedback do the products of the testes have? Where do they act?

A

Negative Testosterone can act on AP and hypothalamus; Inhibin only on AP (FSH)

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18
Q

What are Leydig cells a source of in testes? How much do they make up in testes?

A

Sex-steroid production; over half by 60 days gestation

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19
Q

What is needed to increase Leydig cells?

A

Maternal chorionic gonadotropin (hCG, early); embryonic leutinizing hormone (LH, late)

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20
Q

For males, what happens at puberty with respect to HP-gonadal axis?

A
  1. Increased number and amplitude of GnRH pulses 2. Sens to neg feedback of testosterone decreases, but more gonadotroph sens to GnRH 3. More LH and FSH production 4. More testosterone; commence spermatogenesis
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21
Q

What cells does FSH bind to? What is stimulated?

A

Sertoli cells; ABP, aromatase, growth factors, inhibin production and gene transcription

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22
Q

What cells does LH bind to?

A

Leydig cells; Involved in biosynthesis of testosterone

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23
Q

What does testosterone feed back on?

A

Hypothalamus and its release of GnRH; AP with LH release

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24
Q

What does inhibin feed back on?

A

AP and release of FSH

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25
Q

What does LH do at cellular level?

A

GPCR, make cAMP, activate PKA 1. testosterone synthesis 2. convert cholesterol to pregnenolone (stimulate) 3. help make sterol carrier protein, sterol activating protein

26
Q

What does FSH do?

A
  1. Increase androgen binding protein (local testosterone kept high) 2. P450 aromatase for estrogen 3. Growth factors to support sperm production 4. Inhibins Secondary effects: Leydig cells; increase sperm motility
27
Q

How do Leydig cells act on Sertoli cells?

A

Testosterone; beta-endorphin inhibits Sertoli cell proliferation

28
Q

How do Sertoli cells interact with Leydig cells?

A

Estrogen; growth factors lead to increased LH receptors on Leydig cells

29
Q

Where do odor receptor cells and GnRH producing cells develop?

A

Olfactory epithelium

30
Q

How do GnRH neurons head into brain and later hypothalamus?

A

Along the neurosensory cell axons

31
Q

What happens if GnRH neurons can’t head back to brain and hypothalamus? What is a defect? What is the main danger?

A

Kallmann Syndrome (hypogonadotropic hypogonadism); congenital anosmia; osteoporosis

32
Q

What gene mutations can lead to Kallman Syndrome?

A

KAL-1 (X-linked); FGFR1 (auto dom); PROK2 and PROKR2

33
Q

What is the rate-limiting step in androgen synthesis? What is it regulated by?

A

Cholesterol to pregnenolone through 20,22 desmolase (SCC enzyme); LH levels

34
Q

What does aromatase do? Where is it located?

A

Conversion of androstenedione and testosterone to estrone and estradiol; Sertoli cells

35
Q

How is DHT made? Where does it occur mostly?

A

From testosterone through 5alpha-reductase; mostly in peripheral tissues

36
Q

What are two deficiencies leading to male pseudohermaphroditism?

A

5alpha-reductase deficiency (low DHT, okay testosterone); androgen insensitivity syndrome (normal testosterone, DHT, no androgen receptors–>Wolffian duct degen; normal levels of AMH)

37
Q

What are the androgenic effects of androgens?

A
  1. Maturation of sex organs (e.g. penis) 2. Secondary sex characteristics 3. Voice deepens, beard grows, axillary hair
38
Q

What are the anabolic effects of androgens?

A

Protein synthesis, tissue growth with androgen receptors, muscle growth, more bone density and strength; males with larger organs; estradiol can promote bone maturation

39
Q

What can estrogens regulate in males?

A

Sex drive and behavior in males

40
Q

What is the biologically active form of testosterone? What receptor does it bind? What has the higher affinity for this receptor?

A

Free form Homodimeric receptor (AR/AR) DHT

41
Q

What does increased testosterone lead to?

A

Increased hematocrit, muscle mass, upper body fat, deeper voice, more LDL and VLDL; also important for Wolffian duct structures

42
Q

What happens in andropause?

A

No abrupt loss of fertility; testosterone decreases with increased age (>40); number and quality of sperm goes down; FSH and LH increase

43
Q

What problems are associated with reduced testosterone (<300 ng/dL very low)?

A

Less bone formation, muscle mass, appetite, libido, hematocrit; sleep disturbances, mood problems, fatigue, loss of body and facial hair

44
Q

Who should not be treated with testosterone?

A

Men with prostate or breast cancer

45
Q

What is used to treat male pattern baldness? Side effects?

A

Finasteride (Propecia): blocks DHT production; impotence, abnormal ejaculation, depression

46
Q

What happens with anabolic steroid abuse?

A
  1. Lower sperm count, testicles shrink 2. Possible heart failure, liver tumors, stroke, kidney failure 3. Irreversible breast enlargement in men 4. women with excess body hair and voice deepening
47
Q

What is Kennedy’s Disease called? What type of disease? Where is the defect? What are symptoms?

A

Spinobulbar Muscular Atrophy LMN disease (CAG repeat expansion leading to polyglutamine expansion in androgen receptor) Gynecomastia, impotence, erectile dysfunction

48
Q

How far does a Sertoli cell cover? What connects them?

A

From basal lamina to seminiferous tubule lumen; tight junctions

49
Q

When is spermatogenesis initiated? By what?

A

At puberty FSH via Sertoli cells; LH-driven increases in testosterone and Sertoli cell growth factors

50
Q

What is required for fully mobile/fertile sperm?

A

Testosterone

51
Q

What does the acrosome do for sperm?

A

Protection; carries enzymes needed to dissolve jelly coat of egg during fertilization

52
Q

What is semen derived from? What do the seminal vesicles provide?

A

Seminal vesicles, bulbourethral glands, prostate; 70% of volume and fructose

53
Q

What processes of the dick does the sympathetic nervous system control?

A

Emission and ejaculation Maintain detumescence

54
Q

What does the parasympathetic nervous system control?

A

Erection (Tumescence)

55
Q

What is responsible for penis somatic innervation? What is the blood supply of the penis?

A

Pudendal nerve and artery

56
Q

How does erection work at a cellular level?

A

Nerve terminals release ACh and NO; NO relaxes smooth muscle (artery vasodilation) and increases IC cGMP levels

57
Q

How does Viagra (Sildenafil) work? What are side effects?

A

Inhibits cGMP-specific phosphodiesterase type 5; blue vision for pilots, or taking vasodilators –> death

58
Q

In terms of circulation, what enables corpora expansion?

A

Smooth muscle relaxation in arterial vasculature –> increased blood flow to fill and dilate sinusoidal spaces; somatic fiber stimulation and expanding cavernosal spaces decrease venous outflow (venous plexus)

59
Q

What is emission? What causes it?

A

Ejaculate into urethra; symp stimulation causes contraction of smooth muscle in glands, epididymis, and vas deferens so semen goes into prostatic urethra

60
Q

What is ejaculation? Why wouldn’t you be able to ejaculate?

A

Spinal reflex through pudendal nerve usually accompanied by orgasm; sex and pharmaco inhibition, ANS malfunction, prostatectomy, ejaculatory duct obstruction

Repro Physio (4 decks)

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