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Endocrinology and Reproduction > Male Reproductive Endocrinology II > Flashcards

Male Reproductive Endocrinology II Flashcards

1
Q

The entire sequence of spermatozoa development requires around

A

60-70 days

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2
Q

This process (termed spermatogenesis) critically depends on support from the surrounding

A

Sertoli Cells

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3
Q

Within the basal compartment of the spermatic tubule (i.e. just beneath the basement membrane), spermatogonium undergo two mitotic divisions giving rise to

A

Three active Cells (Ap) and one resting cell (Ad)

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4
Q

The single resting AD cell will eventually serve a the progenitor for a later generation of

A

Sperm

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5
Q

The active Ap cells divide further to generate type B spermatogonia, which then give rise to a number of

A

Primary spermatocytes (PL)

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6
Q

These cells then enter the prophase of meiosis followed by the first

A

Reduction division

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7
Q

During this period, the complicated process of synapsis and chromosomal crossover occur. Within the adluminal compartment, we see the division of their daughter cells which are termed

A

Secondary spermatocytes

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8
Q

Their products, termed spermatids, contain 22 autosomes and either an

A

X or Y chromosome

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9
Q

The spermatids lie near the lumen of the tubule and are attached to the abutting Sertoli cells by

A

Specialized Junctions

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10
Q

In the final process of spermatogenesis, called spermiogenesis, spermatids undergo nuclear condensation, shrinkage of their cytoplasm, formation of an acrosome cap, and development of a

A

Flagellum

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11
Q

The spermatozoa are then extruded into the tubular lumen while most of the cytoplasm remains imbedded in Sertoli cells as

A

Residual Bodies

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12
Q

Movement of the spermtozoa into the epididymis is facilitated by fluid currents generated by the

A

Peritubular myoid cells

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13
Q

Contains the nucleus with its haploid chromosome content, and the acrosomal cap

A

Head of spermatozoa

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14
Q

Has concentrated hydrolytic and proteolytic enzymes that facilitate penetration of the ovum

A

Acrosomal cap

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15
Q

The middle peice,or body, of the mature spermatozoa contains the

A

Mitochondria

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16
Q

Contains stored ATP and pairs of contractile microtubules down its entire length

A

Principle peice of the flagellum

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17
Q

Cross-bridging arms contain

A

Dynein

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18
Q

An ATPase that transfers the energy of ATP into a sliding movement between the microtubules that imparts a flagellar motion to the spermatozoa

A

Dynein

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19
Q

For normal sperm production to occur, we must have normal function of the

A

HPT axis

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20
Q

Men with congenital GnRH, or FSH.LH deficiency are

A

Infertile

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21
Q

Therapeutic administration of GnRH or LH/FSH can restore

A

Spermatogenesis

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22
Q

Has the primary role of stimulating Leydig cells to produce testosterone

A

LH

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23
Q

Clearly stimulates Sertoli cells and this is likely the principal means by which it promotes spermatogenesis

A

Testosterone

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24
Q

Specifically, testosterone acts in conjunction with FSH to regulate

A

Sertoli Cell function

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25
Q

What are six examples of proteins that are upregulated in the Sertoli cells under the influence of FSH and testosterone?

A
  1. ) Inhibin
  2. ) AR
  3. ) Androgen-binding protein (ABP)
  4. ) Iron, copper, and Vitamin A BPs
  5. ) Growth factors
  6. ) Proteases and plasminogen activator
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26
Q

Modulates FSH release from pituitary gonadotrophs

A

Inhibin

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27
Q

Regulates specific gene expression in Sertoli cells in response to high levels of androgens

A

AR

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28
Q

Binds testosterone, DHT, and estradiol with high affinity and keeps their concentration high in the testes

A

ABP

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29
Q

Is also thought to facilitate the entry of androgens into sperm by endocytosis where androgens may influence spermatogenesi s

A

ABP

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30
Q

Concentrate their ligands in the testes where they promote sperm production

A

Iron, Copper, and Vitamin A BPs

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31
Q

Act in a paracrine manner to stimulate mitosis and inhibit apoptosis of spermatogonia

A

Growth factors like IGF 2, stem cell factor, epidermal growth factor (EGF), and TGF-β

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32
Q

Promote spermiation by facilitating (mechanically or chemically) the entry of spermatozoa into the lumen

A

Proteases and Plasminogen Activator

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33
Q

Spermatogenesis is further regulated in a paracrine fashion via local feedback loops between

A

Leydig, Sertoli, and peritubular cells

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34
Q

For example, testosterone from Leydig cells can stimulate the growth and differentiation of

A

Peritubular cells

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35
Q

These peritubular cells in turn secrete growth factors that stimulate

A

Sertoli Cells

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36
Q

Similarly, estradiol secreted from Leydig cells positively effects Sertoli cells and developing sperm, all of which express

A

Estrogen Receptors

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37
Q

The functional activity and shape of Sertoli cells changes during spermatogenesis suggesting that Sertoli cells respond to signals from

A

Sperm

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38
Q

One candidate sperm cell signaling factor is

A

Tumor necrosis factor α (TNFα)

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39
Q

Notably, Sertoli cells express

A

TNFα-receptors

40
Q

In adults, plasma testosterone levels exhibit small pulses throughout the day corresponding to pulses of

A

LH

41
Q

Much of the circulating testosterone is converted into the more potent androgen, DHT in target tissues (e.g., the prostate gland) via the enzyme

A

5α-reductase

42
Q

DHT is more potent than testosterone in that it has a higher affinity for the

A

Androgen Receptor

43
Q

Also secreted in large amounts by Leydig cells but possesses relatively weak intrinsic biological activity

A

Androstenedione

44
Q

The major sources of estradiol and estrone in men

A

Testosterone and androstenedione

45
Q

Only about 10% of these estrogenic compounds are directly secreted by the testes. Most of the estrogen in males is produced from circulating testosterone and androstenedione that become aromatized via

A

Aromatase

46
Q

About 65% of circulating testosterone is bound to a liver-derived glycoprotein termed

A

Sex-hormone binding globulin (SHBG)

47
Q

SHBG is identical in amino acid sequence to ABP of the Sertoli cells; SSBG and ABP differ in terms of their

A

Post-translational glycosylation

48
Q

The remaining 33% of circulating testosterone is bound to

A

Serum Albumin

49
Q

Also binds DHT and a substantial fraction of circulating estradiol

A

SHBG

50
Q

Are not immediately biologically active but rather, serve as mobile reservoirs of androgen for peripheral tissues

A

Testosterone bound to SHBG

51
Q

SHBG concentration is itself decreased by androgens and increased by

A

Estrogens

52
Q

Hence, androgens are believed to increase their own biological availability by increasing the levels of

A

Unbound Hormone

53
Q

Only about 1% of the total daily production of testosterone is directly

A

Excreted

54
Q

Is believed to be initially responsible for stimulating testosterone production from fetal Leydig cells

A

Human Chorionic Gonadotropin (hCG)

55
Q

After the sixth decade of life, plasma testosterone levels begin to decline primarily due to the gradual loss of responsiveness of Leydig cells to

A

LH stimulation

56
Q

Note that the loss of testosterone-induced negative feedback allows

A

LH/FSH levels to rise during this period

57
Q

Testosterone enters target cells by

A

Passive diffusion

58
Q

If the target cell expresses CYP19, testosterone can also be converted into estradiol, a ligand for the

A

Estrogen Receptor (ER)

59
Q

In the absence of ligand, the AR resides in the cytoplasm in an inactive state complexed with

A

Heat shock proteins

60
Q

In the presence of DHT or testosterone, the receptor translocates to the nucleus, homodimerizes and then binds to specific DNA sequences termed

A

Androgen Response Elements

61
Q

Crucial during fetal development for the masculinization of the Wolffian ducts into the epididymis, vas deferens, and seminal vesicles

A

Testosterone (not DHT)

62
Q

Subsequently, the conversion of testosterone into DHT is required for the further fetal development of the

A

Penis, scrotum urethra, and prostate

63
Q

At puberty, the hypothalamus begins to secrete increasing amounts of

A

GnRH

64
Q

Are both required at puberty for the enlargement of the penis and for further development of the testes and seminal vesicles

A

Testosterone and DHT

65
Q

Recall that development and growth of the testes at puberty also requires the orchestrated action of

A

FSH and LH

66
Q

Is again required at puberty for the development of the scrotum and prostate, and to stimulate hair follicles to produce the typical male patterns of facial, pubic and body hair

A

DHT

67
Q

Stimulates the production of sebum fro the sebaceous gland

-likely explains acne during puberty

A

DHT

68
Q

Can promote male pattern baldness in the scalp of fully grown adults

A

DHT

69
Q

Mediates enlargement of the larynx and thickening of the vocal cords during puberty that results in a deeper voice

A

Testosterone

70
Q

First promotes bone lenghtening during puberty, but ultimately terminates linear growth by closing epiphyseal growth centers

A

Testosterone

71
Q

Importantly, bone producing cells, termed osteoblasts, express both

A

AR and ER

72
Q

Testosterone and estrogen potentiate growth hormone secretion and subsequently synergize with growth hormone by stimulating the production of various growth factors and cytokines in

A

Osteoblasts

73
Q

Testosterone administration in adults results in nitrogen retention, indicating

A

Protein anabolism

74
Q

Does not increase the muscle cell number, but rather it increases the size of the muscle fibers

A

Testosterone

75
Q

In humans, the principle androgen-sensitive muscles are those of the

A

Pectoral region and shoulders

76
Q

Increases plasma levels of low-density and very-low density lipoproteins (LDLs and VLDLs), while at the same time testosterone decreases circulating levels of high-density lipoproteins (HDLs)

A

Testosterone

77
Q

Testosterone also promotes fat distribution in the

A

Upper body

78
Q

Maintains normal red blood cell mass by stimulating erythropoetin synthesis and this matruration of erythroid precursors

A

Testosterone

79
Q

Testosterone inhibits the hepatic expression of

A

Nuclear hormone carrier proteins

80
Q

Occurs in both familial and sporadic forms and can be inherited as an autosomal dominant, autosomal recessive, or an X-linked trait

A

Congenital Gonadotropin Deficiency

81
Q

The underlying inherited genetic defects can be manifold and include mutations in the

A

GnRH receptor, LHβ and FSHβ genes

82
Q

Elevated levels of cortisol inhibit LH secretion in

A

Cushing’s syndrome

83
Q

Along these same lines, fasting or critical illnesses (situations where cortisol levels go up and could remain high) can also cause

A

Gonadotropin Deficiency

84
Q

The most common genetic cause of hypogonadism in men is

A

Klinefelter’s Syndrome

85
Q

Characterized by abnormally small testes, elevated gonadotropin levels, impaired male sexual development, impaired spermatogenesis (azoospermia) and\ gynecomastia

A

Klinefelter’s syndrome

86
Q

The unerlying genetic defect in Klinefelter’s syndrome is the presence of an

A

Extra X chromosome (47, XXY)

87
Q

A variant of Klinefelter’s syndrome but is more rare

A

XX mle syndrome

88
Q

In approximately 80% of 46, XX men, a fragment of the SRY has been translocated to the

A

X chromosome

89
Q

In 46, XX men lacking Y chromosome fragments, we see the presence of a duplicated

-indicates autosomal mechanism

A

SOX9 gene

90
Q

A downstream target of SRY-mediated testicular development

A

SOX9

91
Q

Severe genetic defects in the LH receptor can result in an autosomal recessive form of male psuedohermaphroditism in which 46, XY individuals have a

A

Female phenotype, blind ending vagina, and inguinal testes w/ no Leydig cells

92
Q

Less severe LH receptor mutations are associated with variable degrees of impaired male sexual development and

A

Low testosterone

93
Q

The most common cause of acquired testicular failure in adults is

A

Viral Orchitis

94
Q

Can be acquired from infection by the mumps virus, echovirus, lymphocytic choriomeningitis virus as well as members of the group B arboviruses

A

Viral Orchitis

95
Q

Cyproterone, the antifungal agent ketoconazole, antiepileptic drugs phenytoin and carbamazepine, or ingestion of large amounts of ethanol, marijuana, heroin or methadone are examples of drugs that cause

A

Low testosterone

96
Q

Inherited genetic defects in genes involved in androgen biosynthesis have been implicated in a number of

A

Male hypogonadal disorders

Endocrinology and Reproduction (15 decks)

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