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SF3-EXAM 4 (CAMELITA) > Physiology of Male Reproductive System > Flashcards

Physiology of Male Reproductive System Flashcards

1
Q

What are the functional compartments of the male reproductive tract?

A

Seminiferous Tubules

  • Exocrine function
  • Germ cells
    • Produce sperm

Interstitial Tissue

  • Endocrine
  • Leydig cells
    • Androgen secretion
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2
Q

Androgens are ________ steroids.

A

C19

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3
Q

Majority of 5-a dihydrotestosterone is formed in _____________.

A

Peripheral tissues

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4
Q

What are the major steroids that are produced by the testis?

A
  • Testosterone
    • ​Activity of 100
  • Androsterone
  • Androstenedione
  • 5-a-dihydrotestoterone
    • ​Activity of 250

NOTE: Some 5-a-dihydrotestosterone is made in the testes but the majority is made in peripheral tissue

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5
Q

How does cholesterol get into the leydig cells?

A
  • De nove synthesis from acetate
  • Cholesterol is brought in by LDL

NOTE: This takes place in the mitochondria of the cell

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6
Q

What is the first step in the synthesis of testosterone from cholesterol?

A
  • Conversion of cholesterol to pregnenolone with CYP11A1 (cholesterol side chain cleavage) enzyme

NOTE: This is the control point for this system

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7
Q

Which protein is responsible for bringing cholesterol into the mitochondria of leydig cells?

A
  • StAR protein
    • ​Stimulated by LH
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8
Q

What are the two loops through which testosterone can be formed from cholesterol? Which loop is most common? What is the pathway for each loop?

A
  • Delta 5 Loop
    • ​Most common
    • Cholesterol-> Pregnenolone-? 17 OH-pregnenolone-> DHEA (dehydroepiandrosterone)-> Androstenediol-> Testosterone
  • Androstenedione
    • ​Cholesterol-> Pregneolone-> Progesterone-> 17-OH-progesterone-> Androstenedione-> Testosterone
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9
Q

__________ is the major source of estradiol in men.

A

Androstenedione

NOTE: Androstenedione may be converted to estrone and subsequently estradiol in peripheral tissue.

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10
Q

What are the major sex steroid binding proteins?

A
  • Testosterone- Estrogen Binding Protein (TEBG)
    • High affinity binding site
    • Distribution in blood: 30-40%
  • Albumin
    • Low affinity binding site
    • Distribution in blood: 50-60%

NOTE: Only about 0.5-3% of testosterone is traveling freely in blood

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11
Q

Which hormone has the highest binding affinity for Testesterone-Estrogen Binding Protein (TEBG)?

A
  • Dihydrotesterone (DHT)- 100
  • Testosterone- 33
  • Estradiol- 25

NOTE: A decrease in TEBG will free up more of the ligand with the highest affinity and less of the ligand with the lowest affinity.

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12
Q

What are two fates of androstenedione?

A

Can be converted to:

  • Testosterone, which can then be converted to:
    • Estradiol
    • Dihyrotestosterone
  • Estrone
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13
Q

Roles of estradiol

A
  • Bone resorption
  • Epiphyseal fusion
  • Sexual differentiation of brain
  • Some behaviors
  • Plasma lipids
  • Atherosclerosis progression
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14
Q

Roles of dihyrdotestosterone

A
  • Prostatic growth
  • Skin
  • Hair follicles in androgen sensitive areas
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15
Q

What is mechanism of testosterone action?

A
  • TBEG attaches to testosterone
  • Testosterone comes off, fuses across the plasma membrane into the cell and is acted on by 5-alpha DHT reductase to form DHT
  • Testetosterone displaces the HSP chaperone from the androgen receptor
  • The androgen receptor is dimerized and phosporylated
  • The androgen receptor and testosterone structure enter the nucleus binds to androgen response elements,collects coactivator proteins and eventually activates target genes to cause the biological response.
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16
Q

What activites are associated with testosterone and dihydrotestosterone?

A
  • Testosterone- receptor
    • ​Feed back regulation of gonadotropin secretion
    • Differentiation of the wolffian duct in utero
  • DHT receptor
    • ​External genitalia differentiation in utero
    • Virilization during puberty

NOTE: Both testosterone and dihydroxytestoserone interact with the androgen receptor

17
Q

There a rings of _______ cells around the semineferous tubules.

A

Sertoli

NOTE: Most of the actions of the testes are in the avascular compartment becuase many blood proteins inhibit spermatogenesis

18
Q

What are the two functional compartments of semineferous tubules?

A
  • Adluminal
    • Sertoli cells
    • Tight junctions
    • Seminal fluid
  • Basal
    • On the outside, where we have spermatogonia and mitosis

NOTE: Migration from the basal to adluminal compartment is where the germ cells hit the avascular zone and meiosis starts. This process is control through Sertoli cells

19
Q

Function of Sertoli cells

A
  • Nourish healthy cells and phagocytize damaged germ cells
  • Synthesize luminal proteins
  • Maintain tubular fluid
  • Convert androgens to estrogens
  • Site for hormonal modulation of tubular function

NOTE: If Sertoli cells are stimulated with FSH the sertoli cell will communicate with gap junctions, allowing for the germ cells to cross the gap junctions.

20
Q

Which hormones are produced by sertoli cells?

A

Estradiol (-)

Inhibin (+)

Activin (-)

*These hormones regulate leydig activity

21
Q

Inhibin and folistatin exert feedback supression while activin shows feedback stimulation of __________ secretion.

A

FSH

22
Q

During hyperprolactinonemia elevated prolactin ___________ (supresses/stimulates) reproduction at the hypothalamic and pituatary levels.

A

Supresses

23
Q

How can the male reproductive (hypothalamic-pituatary) axis system be assessed?

A
  1. Using clomid
  • Clomid is a weak estrogen agonist in most places
  • At the anterior pituatary it is a strong estrogen antagonist that can block a lot of the feedback
    • Clomid blocks access to the receptor without activating it
  1. By blocking feedback, this allows GnRH to go up and we measure a rise in LH and FSH
    * Measures to see if the axis is working properly
  2. Injection of HCG
  • Let’s you know how well the testes are working
  • Measure the rise in testosterone being produced
24
Q

During erection, smooth muscles are _______ (relaxed/contracted).

A

Relaxed

*Sinusoidal spaces are filled, outflow venules are compressed against the tunica albuginea

25
Q

What are the mechanism of penile erection?

A
  1. Relaxation of trabecular smooth muscle
  • Parasympathetic input
  • Decrease in intracellular Ca2+
  • Increase in PGE1
  • Increase in NO
  • Decrease in smooth muscle sensitivity to Ca2+
  1. Increased blood flow into cavernosal sinusoids
  2. Engorged corpora cavernosa presses venules against tunica albuginea restricting venous outflow
26
Q

Which pathologies lead to gynecomastia?

A
  • Hypogonadism- Klinefelters
  • Chronic liver disease
    • Tend to get an increase of TEBG secretion, which takes testosterone out of circulation
  • Thyrotoxicosis
  • Neoplasia
  • Drugs

NOTE: Anytime there is an elevation of estrogen that’s insufficiently blocked by androgens we can see expression of estrogenic activity.

27
Q

What is the major cause of gynecomastia?

A
  • Increased estrogen/androgen ratio (either increased estrogen and/or decreased androgen can accomplish)

NOTE: Gynecomastia can be physiological, pathological, or idiopathic.

28
Q

What are the 4 types of pathological gynecomastia?

A
  • Deficient testosterone formation
  • Increased estrogen secretion
  • Increased extraglandular estrogen formation-Increased substrate
  • Increased extraglandular estrogen formation- increased aromatase enzyme

SF3-EXAM 4 (CAMELITA) (23 decks)

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