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Endocrinology > Exam 3 Lecture 21 Male Reproductive System > Flashcards

Exam 3 Lecture 21 Male Reproductive System Flashcards

1
Q

Describe the hypothalamus-anterior pituitary- gonads axis

A

The hypothalamus GnRH, which travels in the hypothalami-pituitary portal vessels to anterior pituitary. The anterior pituitary responds by secreting LH and FSH. FSH and LH travel to the gonads, where they stimulate both the secretion of sex hormones and the synthesis of gametes. The sex hormones will travel to reproductive tract and other organs. They will also offer negative feedback to the hypothalamus and the anterior pituitary, in most cases, except estrogen in the female menstrual cycle.

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2
Q

What are the main components of the male reproductive system?

A

Testes, epididymis, penis (including urethra), and ductus deferens

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3
Q

What are the accessory glands of the male reproductive system?

A

Seminal vesicles, prostate, bulbourethral glands, urethral glands

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4
Q

What role does testosterone play in spermatogenesis? Through which cells does it act.

A

It is required for its initiation and maintenance. It acts through the Sertoli cells.

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5
Q

How does testosterone affect GnRH secretion?

A

It provides negative feedback to the hypothalamus, which decreases GnRH secretion.

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6
Q

How does testosterone affect LH secretion?

A

It inhibits LH secretion via a direct action on the anterior pituitary.

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7
Q

How does testosterone affect male accessory reproductive organs?

A

It induces their differentiation and maintains their functions.

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8
Q

How does testosterone affect male secondary sex characteristics?

A

It induces them. It opposes action of estrogen on breast growth.

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9
Q

How does testosterone affect anabolism and bone growth?

A

It stimulates protein anabolism, bone growth, cessation of bone growth.

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10
Q

How does testosterone affect sex drive and aggression?

A

It is required for the former and may enhance the latter.

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11
Q

How does testosterone affect the quantity of red blood cells?

A

It stimulates erythropoietin secretion by the kidneys.

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12
Q

Inside the testes, what do you find?

A

Seminiferous tubules enclosed by septum, septum surrounded by tunica albuginea, tubule recti at the origin of the seminiferous tubules, the rete testis and mediastinum testis facing the epidymis.

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13
Q

What surrounds the testes?

A

tunica vaginalis

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14
Q

What connects the testes to the epididymis?

A

the ductuli efferentes

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15
Q

What are the three parts of the epididymis?

A

head, tail and body

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16
Q

After epididymis, through what do gametes travel?

A

ductus deferens

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17
Q

what cells surround the seminiferous tubules?

A

myoid cells

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18
Q

what cells are in the interstitium of the testes?

A

Leydig cells

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19
Q

what layers make up the seminiferous tubule?

A

from inside out, lumen, seminiferous epithelium, lymphatic channel, and wall of seminiferous tubule

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20
Q

where are spermatogenic cells located?

A

in the seminiferous epithelium

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21
Q

where are sertoli cells located?

A

in the seminiferous epithelium

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22
Q

what can be found in the inter tubular space?

A

venules and arterioles, leydig cells, and macrophages

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23
Q

what kind of cells are sertoli cells?

A

somatic

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24
Q

what are the spermatogenic cells?

A

spermatogonia, spermatocytes and spermatids

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25
what is in the wall of the seminiferous tubule?
fibroblasts and myoid cells
26
How does cholesterol become an androgen?
cholesterol becomes pregnenolone via SCCE, then through 17alpha hydroxylase, becomes 17-OH pregnenolone, then through 17-lyase, it becomes DHEA, then through 3beta HSD it becomes androstenedione, then through 17beta HSD, it becomes testosterone, then through aromatase, it becomes estradioi
27
how does cholesterol become progesterone?
SCCE to pregnenolone, 3beta HSD to progesterone
28
how does progesterone become an androgen?
17alpha hydroxylase to 17-OH progesterone, 17-lyase to androstenedione, 17beta HSD to testosterone, aromatase to estradiol
29
How does testosterone become the derivative 5alpha-dihydrotestosterone?
through 5alpha-reductase
30
How does testosterone become the derivative 5alpha-dihydrotestosterone?
through 5alpha-reductase
31
Where are Leydig cells found?
In the inter tubular space of the testes.
32
Like all steroid-producing cells, Leydig cells have abundant what?
lipid droplets smooth endoplasmic reticulum mitochondria with tubular cristae
33
what two hormones regulate Leydig cell function?
1. LH, which stimulates testosterone production | 2. Prolactin, which induces the expression of the LH receptor
34
What does prolactin do?
it induces the expression of the LH receptor
35
how does StAR regulate the synthesis of steroids?
it transports cholesterol across the outer mitochondrial membrane
36
A mutation in the gene encoding StAR can lead to what pathology?
defective synthesis of adrenal and gonadal steroids or lipid congenital adrenal hyperplasia
37
What do Leydig cells produce?
testosterone
38
Where does testosterone go from Leydig cells?
lymphatic sinusoid and blood vessel
39
what are the keys to the nine functions of the Sertoli cells?
chemicals, developing sperm, luminal fluid, sperm proliferation and differentiation, inhibin, Leydig cell function, defective sperm, MIS
40
what does Sertoli cell provide to chemicals in plasma?
barrier
41
How does Sertoli cell respond to testosterone and FSH stimulation?
secretes paracrine agents that stimulate sperm proliferation and differentiation
42
what is the role of inhibin?
inhibits FSH secretion from pituitary
43
How does Sertoli cell influence Leydig cell function?
secretes paracrine agents
44
What does Sertoli cell do to defective sperm?
phagocytose it
45
what is Mullerian inhibiting substance (MIS)?
it causes primordial female duct system to regress
46
when does Sertoli cell secrete MIS?
during embryonic life
47
what does Sertoli cell do to developing sperm?
nourish it
48
what does Sertoli cell do with retinoic acid and its derivatives?
stores them.
49
What are retinoic acid and its derivatives necessary for?
sperm development
50
What are the spermatogenesis stages?
primordial germ cell 2n --> spermatogonia 2n --> primary spermatocytes 2n --> secondary spermatocytes n --> spermatids n --> spermatozoa
51
How do primordial germs cells become spermatogonia?
they migrate from yolk sac to testes and differentiate
52
How do spermatogonia 2n become 1º spermatocytes?
they proliferate by mitosis. B type differentiates into spermatocytes that are primary.
53
How do 1º spermatocytes differentiate into secondary spermatocytes?
they undergo 1st meiotic division
54
How do secondary spermatocytes become spermatids?
they miss S phase and undergo 2nd maturation division
55
how do spermatids become spermatozoa?
they transform, without dividing
56
How many primary spermatocytes does spermatogonium give rise to?
16 primary spermatocytes
57
How may spermatides are given rise to by primary spermatocytes?
four
58
How many spermatozoa do spermatides give rise to?
four
59
what are the three main functions of the epididymus?
a. sperm maturation b. sperm storage c. sperm transport
60
how does the epididymus participate in sperm maturation?
a. stabilization of condensed chromatin | b. changes in plasma surface proteins
61
what are the functions of the accessory glands of the male reproductive system?
a. nutrients b. buffers c. chemicals d. prostaglandins
62
what do buffers produced by accessory glands do?
they protect sperm from acidic environment
63
what do chemicals released by accessory glands do?
they increase sperm motility
64
what kind of receptor is the androgen receptor?
nuclear hormone receptor
65
what happens after AR binds androgens as ligands?
a. dissociates from chaperone HSP90 b. self-dimerizes c. translocates to nucleus
66
From N-terminal to C-terminal, what are the parts of the androgen receptor?
NTD, DBD, hinge, blank, AF-2, blank. LBD hovers over AF-2.
67
What is NTD? what factor is at NTD?
N-terminal domain. Activating factor-1.
68
What is AF-2?
activation function-2
69
what does C-terminal domain divide into?
LBD and CTE, which is C-terminal extension
70
When testosterone enters a target cell, what does it do?
it binds with receptor in nucleus directly, or it turns into dihydrotestosterone via 5alpha-reductase and binds with the androgen receptor.
71
What does testosterone propagate after binding with receptor?
a. gonadotropin regulation b. spermatogenesis c. sexual differentiation/Wolffian stimulation/external virilization
72
What does dihydrotestosterone propagate after binding with receptor?
a. external virilization | b. sexual maturation at puberty
73
Lower peripheral level testosterone functions? (6)
CNS differentiation, genital differentiation, sexual characteristics, accessory sex glands, anabolic and general metabolic processes, behavior/libido
74
what genital differentiation does lower peripheral testosterone help with?
genital apparatus and genital excurrent duct system
75
How does lower peripheral testosterone help secondary sexual characteristics?
growth and maintenance
76
How does lower peripheral testosterone help accessory sex glands?
growth and maintenance
77
What is prostate-specific antigen (PSA)?
a valuable marker for the early detection of prostate cancer?
78
what is benign prostatic hyperplasia?
noncancerous enlargement caused by DHT, a metabolite of testosterone.
79
what is DHT?
a metabolite of testosterone. It induces growth factor expression that drives tissue enlargement.
80
What does carcinoma of the prostate depend on?
DHT
81
How can carcinoma of the prostate growth be controlled?
by reducing androgen levels
82
How can androgen levels be reduced when treating carcinoma of the prostate?
a. GnRH antagonist b. estrogen c. surgery d. radiotherapy
83
How can we block AR at N-terminal?
with EPI-001, which interacts with AR NTD to block AR transcriptional acidity through this domain.
84
How can we block AR at ligand binding domain (LBD)?
a. androgen ablation b. antiandrogens c. DHT d. dihydrotestosterone
85
what are the most commonly used therapies in metastatic prostate cancer?
androgen deprivation
86
How does androgen deprivation happen?
medical (LHRH agonists), surgical castration, disruption of androgen binding to AR
87
what do most prostate cancers evolve into?
castration-resistant state
88
Resistance mechanisms to metastatic prostate cancer?
AR, gene mutation or amplification, ligand independent activation or AR and persistent intraprostatic androgens
89
what causes disorder of androgen synthesis?
defects or mutations in enzymes involved in corticosteroid and androgen production
90
what do disorders of androgen synthesis cause?
adrenal insufficiency and pseudohermaphroditism
91
what is impaired androgen production a result of?
mutation in the gene encoding the receptor of LH
92
what do 5alpha-reductase deficiency result in?
female-like external genitalia in males due to lack of dehydrostestosterone.
93
what do androgen receptor defects cause overall?
overall female appearance in the 46, XY males
94
AAS
commonly used substrate to improve exercise performance and /or body image of an athlete.
95
How are AAS used?
in combo with other substances to increase anabolic/performance-enhancing effect

Endocrinology (21 decks)

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