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
Testosterone in Leydig cells get secreted in to
1. Lumen : binding to ABP | 2. Circulation through the peritubular capillary network bound by SHBG and albumin
26
How do Leydig cells get cholesterol to make testosterone
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
27
Free cholesterol —> Pregnenolone done by what enzyme | Regulated by
CYP450SCC (*Cholesterol Desmolase) | LH = more conversion (*increases affinity of P450scc to cholesterol + activates the enzyme) —————> RLS
28
How are androgens and testosterone secreted
In the urine 50% as 17ketosteroids Others as conjugated androgen Others as diol/triol derivatives
29
When does testosterone develop in fetus if is going to be a male
2nd month
30
Testosterone in fetal development does creates what and causes what
Makes : epididymis, vas deference, efferent ductile, seminal vesicle CAUSES : descends of testes into scrotum during month 2-3
31
No testosterone is growing male fetus
Cryptorchidism : testis don’t descend
32
Testosterone function during male puberty
1. Deepening voice, growth spurt, increased muscle 2. Closure of epiphyseal plate, 3. Growth of penis, seminal vesicles, spermatogenesis starts, Libido
33
DHT function in fetus
External male genitalia (penis, scrotum, prostate) Male hair distribution + pattern baldness in males Sebaceous glands
34
When do you usually use 5a-reductase inhibitor
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
Benign Prostatic Hypertrophy Sx: 4 of them And REASON males get this
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
What stimulates the Leydig cells
LH with the cAMP-PKA pathway ——> cholesterol to be made(steroidogensis) to make testosterone * has CYP450SCC *also has CYP19
37
What stimulates the Sertoli cells
FSH and testosterone by cAMP-PKA pathway | = makes Inhibins, ABP, CYP19, growth factors
38
Supportive functions of Sertoli cells
Maintain BTB Phagocytosis Transferrin,lactate, Fr transfer to sperm from blood Stimulated by FSH
39
Exocrine functions of Sertoli cells
1. Produce sperm fluid 2. ABP made, 3. Determines when sperm can be released in to lumen
40
Endocrine functions of Sertoli cells
1. Express ABPR, TR, FSHR 2. Makes anti-mullerian H. (AMH) 3. Makes estrogen *CYP19 -aromatase 4. Makes inhibin to regulate FSH
41
Inhibin
Negative regulator to FSH
42
What is the negative regulator for LH
Androgens - from Leydig cells
43
What is the negative regulator for FSH
Inhibin - from Sertoli cells
44
Spermatogonia are what type of cell
Diploid 2N | * mitosis , some start meiosis 1
45
Primary Spermatocytes are what type of cell
Diploid 4N | * during meiosis 1 (replicated)
46
Secondary spermatocytes are what type of cells
Haploid 2N | * finished meiosis 1, some starts meiosis 2
47
Spermatozoa are what type of cell
Haploid 1N | * finished meiosis 2
48
steps from primordial cells to spermatozoa
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
3 hormones that influence spermatogenesis
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
Exogenous androgens administered causes what
HIGH circulating testosterone | large negative feedback causing LOW GnRH + LH + interstitial T + spermatogenesis
51
Normal levels or testosterone
Low in blood and higher interstitially in testis to make spermatogenesis
52
3 stages in life when there is a testosterone spike where it increases
1. Fetus (2nd trimester) 2. Neonatal ( around 4-6mo) 3. During Puberty (14yo) increases into adulthood-50yo =*sprematogenesis increases with this until 60yo
53
How long do sperm spend on average in epididymis
On average a month
54
What exactly happens when the sperm matures in the epididymis
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
Seminal Vesicle Function : secretes
Mucoid material = nutrients + prostaglandins + fibrinogen
56
What does the prostaglandins do that is secreted around the sperm and in the sperm fluid
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
Function of the prostate gland : what does it secrete
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
Semen is fluid from these 4 glands
1. Vas deference 2. Prostate 3. Seminal Vesicles 4. Bulbourethral gland PH 7.5
59
How long do sperm live ones ejaculated (in body temperature)
24hr-48hr
60
4 sections of the urethra in male
Pre-prostatic urethra Prostatic urethra Membranous urethra Penile urethra
61
Residual Body
Left behind when the sperm is released into lumen and phagocytized by Sertoli cells
62
Flaccid penis vasculature SM
SM are constricted to lower BF into penis
63
Erection
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
what further promotes erection
Somatic stimulation which causes contraction of the base of penis muscles
65
Emission
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
Destruction of this sphincter from prostatectomy
Retrograde ejaculation
67
Ejaculation
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
What causes capacitation of sperm
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
X Testosterone | 2nd-3rd month of gestation
Ambiguous genitalia
70
X testosterone | 3rd trimester
X testicular descent (cryptorchidism) + micropenis
71
X testosterone | Puberty
Poor secondary sexual characteristics | - eunuchoid features (prepubertal characteristics persist, usually opposite sex looking)
72
X testosterone | Post -puberty
``` Low libido Erectile dysfunction Low facial hair, body hair Low energy Infertility ```
73
Kallman’s syndrome
GnRH neurons DONT ——> hypothalamus during embryo = delayed or absent puberty + X smell = Secondary Hypogonadism , more frequent in males
74
Klinefelter Syndrome
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
Testicular Dysfunction
Klineferlters syndrome Low Testosterone Primary hypogonadism
76
Pituitary Dysfunction
low LH and Low FSH | Secondary Hypogonadism
77
Hypothalamic Dysfunction
Kallmann’s Dysfunction Low GnRH Secondary Hypogonadism
78
Hyperprolactinemia
PROLACTIN (for the breasts) ——I GnRH | =Low FSH + LH for the ovaries
79
Prostate Cancer treatment
1. Androgen Receptor antagonist 2. Radiotherapy 3. Radical Prostatectomy
80
Sx: testis tumor in interstitial cells
Large amount of testosterone made
81
As men age what happens
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
Aging and testosterone
Declines after 40yo | DECREASES : bone mass, muscle mass, facial hair, appetite, libido