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GIGU Exam 2 > Male Reprodctive Physiology > Flashcards

Male Reprodctive Physiology Flashcards

1
Q

When in the fetus are the gonads officially either female or male

A

Week 6-7 - testis

Week 9 - Ovaries

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2
Q

Hormones determine the

A

Phenotypic sex

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3
Q

The Sertoli cells secrete

The Leydig cells secrete

A

Anti-mullerian H.

Testosterone

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4
Q

Gonadopropin is released the most when

A

A small spike in fetus
Most in senescence (more in female)
And high up and downs in adult reproductive stage (male is steady straight line)
* increase is puberty

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5
Q

When is FSH or LH higher

A

LH higher : adult reproductive stage

FSH higher : childhood and Senescence

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6
Q

Gonadopropin stimulates

A

GnRH——> LH and FSH *pulsitile ——> testosterone +estrodiol

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7
Q

Estradiol and testosterone do what main function

A

Establish secondary sex characteristics

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8
Q

Administrating GnRH in intermittent pulses

A

Initiates puberty

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9
Q

Administering GnRH continuously long-term

A

No puberty initiated

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10
Q

Testis 2 main functions

A

Secrete testosterone
Spermatogenesis
* need cold temperatures

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11
Q

Epididymis main function

A

Store (short-term) and maturation of sperm

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12
Q

Vas deference funcition

A

Carries the sperm to the ejaculatory duct when seminal vesicle adds to it
Another storage place for sperm in the ampulla

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13
Q

What makes up the epithelium of the seminiferous tubule

A

Sertoli cells

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14
Q

In the adult testis how much of it contains seminiferous tubules

A

80%

And 20% CT with Leydig cells

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15
Q

What 3 Hs. Do the testis secrete

A
  1. Testosterone—> DHT eventually in target tissues
  2. DHT (dihydrotestosterone)
  3. Androstenedione
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16
Q

What enzyme is found in the testis especially the Leydig cells

A

*17B-hydroxysteroid dehydrogenase : androstenedione—> Testosterone
(NO 21Bhydroxylase, NO 11Bhydroxylase = no cortisol+aldosterone, no DHEA)

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17
Q

What concentrates testosterone in the lumen of the seminiferous tubules

A

Testosterone binds to ABP (androgen binding protien)

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18
Q

Which tissues need testosterone to be in the DHT form to have it as an active form
And what enzyme do they have

A

5a- reductase (in peripheral tissue)

Prostate gland, external genitalia, skin, liver

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19
Q

What binds to circulating testosterone

A

Albumin (38%) or SHBG(60%) (Sex-H.-Binding Globulin)

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20
Q

No 5a-reductase

A

Ambiguous external genitalia

* No DHT - important in puberty

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21
Q

What binds to androgen with the highest affinity

A

DHT more then testosterone

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22
Q

Where in testis is estrogen made in the male and for what reason

A

In the Sertoli cells in the seminiferous tubules—> lumen to help spermatogenesis
*CYP19 used testosterone——> estradiol
(Cholesterol—>Androstenedione—> T——> E)

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23
Q

Where is most of male estrogen made

A

80% of male estrogen made in adipose tissue

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24
Q

Where in the Leydig cell is testosterone made and what is the RLS

A

In the mitochondria

RLS :Cholesterol ——CYP450SCC——> Pregnenolone

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25
Q

Testosterone in Leydig cells get secreted in to

A
  1. Lumen : binding to ABP

2. Circulation through the peritubular capillary network bound by SHBG and albumin

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26
Q

How do Leydig cells get cholesterol to make testosterone

A
  1. Make de novo (from LDL + HDL)
    Uses these to make free cholesterol *by HSL (H. Sensitive Lipase)
  2. Free -cholesterol —> mitochondria *bound by StAR
  3. Free- cholesterol —> Pregnenolone * CYP450SCC
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27
Q

Free cholesterol —> Pregnenolone done by what enzyme

Regulated by

A

CYP450SCC (*Cholesterol Desmolase)

LH = more conversion (*increases affinity of P450scc to cholesterol + activates the enzyme) —————> RLS

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28
Q

How are androgens and testosterone secreted

A

In the urine
50% as 17ketosteroids
Others as conjugated androgen
Others as diol/triol derivatives

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29
Q

When does testosterone develop in fetus if is going to be a male

A

2nd month

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30
Q

Testosterone in fetal development does creates what and causes what

A

Makes : epididymis, vas deference, efferent ductile, seminal vesicle
CAUSES : descends of testes into scrotum during month 2-3

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31
Q

No testosterone is growing male fetus

A

Cryptorchidism : testis don’t descend

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32
Q

Testosterone function during male puberty

A
  1. Deepening voice, growth spurt, increased muscle
  2. Closure of epiphyseal plate,
  3. Growth of penis, seminal vesicles, spermatogenesis starts, Libido
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33
Q

DHT function in fetus

A

External male genitalia (penis, scrotum, prostate)
Male hair distribution + pattern baldness in males
Sebaceous glands

34
Q

When do you usually use 5a-reductase inhibitor

A

X DHT = no growth in prostate and baldness
So use for hair loss in male or Benign Prostatic Hypertrophy
*testosterone has no effect on these

35
Q

Benign Prostatic Hypertrophy
Sx: 4 of them
And REASON males get this

A

80% males get this by age 80

  1. Urination increase, especially at night
  2. Difficult initiation urinating and maintaining stream
  3. Involuntary leakage of urine
  4. Postvoid test - measures amount of urine left after peeing
    * have higher numbers of DHT receptors in prostate (NOT MORE DHT H.)
36
Q

What stimulates the Leydig cells

A

LH with the cAMP-PKA pathway ——> cholesterol to be made(steroidogensis) to make testosterone * has CYP450SCC
*also has CYP19

37
Q

What stimulates the Sertoli cells

A

FSH and testosterone by cAMP-PKA pathway

= makes Inhibins, ABP, CYP19, growth factors

38
Q

Supportive functions of Sertoli cells

A

Maintain BTB
Phagocytosis
Transferrin,lactate, Fr transfer to sperm from blood
Stimulated by FSH

39
Q

Exocrine functions of Sertoli cells

A
  1. Produce sperm fluid
  2. ABP made,
  3. Determines when sperm can be released in to lumen
40
Q

Endocrine functions of Sertoli cells

A
  1. Express ABPR, TR, FSHR
  2. Makes anti-mullerian H. (AMH)
  3. Makes estrogen *CYP19 -aromatase
  4. Makes inhibin to regulate FSH
41
Q

Inhibin

A

Negative regulator to FSH

42
Q

What is the negative regulator for LH

A

Androgens - from Leydig cells

43
Q

What is the negative regulator for FSH

A

Inhibin - from Sertoli cells

44
Q

Spermatogonia are what type of cell

A

Diploid 2N

* mitosis , some start meiosis 1

45
Q

Primary Spermatocytes are what type of cell

A

Diploid 4N

* during meiosis 1 (replicated)

46
Q

Secondary spermatocytes are what type of cells

A

Haploid 2N

* finished meiosis 1, some starts meiosis 2

47
Q

Spermatozoa are what type of cell

A

Haploid 1N

* finished meiosis 2

48
Q

steps from primordial cells to spermatozoa

A

Primordial cells -> (gonads)spermatogonia(2N, D) —mitosis—> primary spermatocytes (4N, D)—meiosis 1 —> secondary spermatocytes (2N,H) —meiosis 2 —> spermatids (1N,H)—spermiogenesis—> spermatozoa

49
Q

3 hormones that influence spermatogenesis

A
  1. LH : for testosterone, division of germ cells and sperm formation
  2. FSH : to Sertoli cells to make and nurse sperm + make estrogen
  3. GH : early division of sperm division + metabolism of the testis
50
Q

Exogenous androgens administered causes what

A

HIGH circulating testosterone

large negative feedback causing LOW GnRH + LH + interstitial T + spermatogenesis

51
Q

Normal levels or testosterone

A

Low in blood and higher interstitially in testis to make spermatogenesis

52
Q

3 stages in life when there is a testosterone spike where it increases

A
  1. Fetus (2nd trimester)
  2. Neonatal ( around 4-6mo)
  3. During Puberty (14yo) increases into adulthood-50yo =*sprematogenesis increases with this until 60yo
53
Q

How long do sperm spend on average in epididymis

A

On average a month

54
Q

What exactly happens when the sperm matures in the epididymis

A
  1. Decapacitation : add molecules on head to protect acrosomal reaction from happening before contact with the egg
  2. Strongly mobile sperm
  • can also store sperm for several months
55
Q

Seminal Vesicle Function : secretes

A

Mucoid material = nutrients + prostaglandins + fibrinogen

56
Q

What does the prostaglandins do that is secreted around the sperm and in the sperm fluid

A
  1. Reacts with cervical mucus to make it less thick so sperm can move
  2. Make backward/reverse peristaltic contractions of uterus and Fallopian tube to move sperm towards ovaries
57
Q

Function of the prostate gland : what does it secrete

A

Thin milky fluid : *during emission stage *alkaline
1. Ca+2
2. Citrate ion + phosphate ion
3. Clotting enzyme
4. Profibrinolysin
= TO NEUTRALIZA VAGINA + OTHER SEMINAL FLUIDS

58
Q

Semen is fluid from these 4 glands

A
  1. Vas deference
  2. Prostate
  3. Seminal Vesicles
  4. Bulbourethral gland
    PH 7.5
59
Q

How long do sperm live ones ejaculated (in body temperature)

A

24hr-48hr

60
Q

4 sections of the urethra in male

A

Pre-prostatic urethra
Prostatic urethra
Membranous urethra
Penile urethra

61
Q

Residual Body

A

Left behind when the sperm is released into lumen and phagocytized by Sertoli cells

62
Q

Flaccid penis vasculature SM

A

SM are constricted to lower BF into penis

63
Q

Erection

A

PARASYMPATHETIC (NO)——> vascular SM (helicine a.)* in cavernous spaces
= NO increases cGMP= lowering of Ca+2 = relaxation of SM in vasculature
= increase BF in, and centric the vein

64
Q

what further promotes erection

A

Somatic stimulation which causes contraction of the base of penis muscles

65
Q

Emission

A

When semen moves from epididymis——> ejaculatory duct
SYMPATHETIC: peristaltic contractions of SM of vas deference which closes the internal sphincter of bladder
*usually starts before ejaculation and during ejaculation

66
Q

Destruction of this sphincter from prostatectomy

A

Retrograde ejaculation

67
Q

Ejaculation

A

Propulsion of sperm out from male urethra from rhyming contractions of bulbospongiosus and ischiocavernous muscles at base of penis (SOMATIC NERVES)
*semen exits rapidly and outwardly through urethra

68
Q

What causes capacitation of sperm

A

Changes in female tract:

  1. Uterine + Fallopian tubes wash away inhibitory factors
  2. Loss of cholesterol on acrosome of sperm
  3. Membrane of sperm is more permeable to Ca+2 = increase motility
69
Q

X Testosterone

2nd-3rd month of gestation

A

Ambiguous genitalia

70
Q

X testosterone

3rd trimester

A

X testicular descent (cryptorchidism) + micropenis

71
Q

X testosterone

Puberty

A

Poor secondary sexual characteristics

- eunuchoid features (prepubertal characteristics persist, usually opposite sex looking)

72
Q

X testosterone

Post -puberty

A 
Low libido
Erectile dysfunction 
Low facial hair, body hair
Low energy
Infertility
73
Q

Kallman’s syndrome

A

GnRH neurons DONT ——> hypothalamus during embryo
= delayed or absent puberty + X smell
= Secondary Hypogonadism , more frequent in males

74
Q

Klinefelter Syndrome

A

Seminiferous tubular dysgenesis
XXY
PHENOTYPICALLY : male
Puberty : GnRH doesn’t induce spermatogenesis and testis growth
Also low androgen, high GnRH = primary hypogonadism
Destroyed seminiferous tubules

75
Q

Testicular Dysfunction

A

Klineferlters syndrome
Low Testosterone
Primary hypogonadism

76
Q

Pituitary Dysfunction

A

low LH and Low FSH

Secondary Hypogonadism

77
Q

Hypothalamic Dysfunction

A

Kallmann’s Dysfunction
Low GnRH
Secondary Hypogonadism

78
Q

Hyperprolactinemia

A

PROLACTIN (for the breasts) ——I GnRH

=Low FSH + LH for the ovaries

79
Q

Prostate Cancer treatment

A
  1. Androgen Receptor antagonist
  2. Radiotherapy
  3. Radical Prostatectomy
80
Q

Sx: testis tumor in interstitial cells

A

Large amount of testosterone made

81
Q

As men age what happens

A
  1. Sensitivity to LH decreases
  2. Androgen production decreases
  3. High amount of LH + FSH made (more FSH)
    * men can maintain reproductive function + spermatogenesis thought life
82
Q

Aging and testosterone

A

Declines after 40yo

DECREASES : bone mass, muscle mass, facial hair, appetite, libido

GIGU Exam 2 (13 decks)

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