Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Bloc I - Reproduction > Aug28 M1,2-Male Reproductive System > Flashcards

Aug28 M1,2-Male Reproductive System Flashcards

1
Q

HPT (testicular) axis with hormones

A
  • h: GnRH (gonadotropin releasing H)
  • p: LH and FSH (gonadotropins)
  • t: steroids and inhibin
  • Feedback
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what ntr controls pulsatile secretion of GnRH

A

kisspeptin, 10 aa peptide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

GnRH charact

A
  • susceptible to proteases

- analogs used for infertility tx, contraception, etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

(imp?) main use of GnRH today

A

prostate cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

how to use GnRH analog as an agonist

A

give in pulsatile fashion (every 60-90 min) (like phgy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

how to use GnRH analog as an antagonist

A

give constant long lived dose (inhibits the gonadotropes = cells in pit making LH, FSH)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

2 parts of LH and FSH (gonadotropins)

A
  • alpha subunit (same in LH and FSH). same gene

- beta subunit (makes the bio specif): two diff genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

half life of FSH vs LH

A

FSH very much longer half life than LH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

why FSH half life long

A

need constant exposure to stim the dev of germ cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

why LH half life short

A

comes out in pulsatile fashion (resp to GnRH pulse).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

FSH fct

A

stim dev of germ cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

LH fct

A

stim steroidogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

R of gonadotropins are what

A

GPCRs with 7 parts TM prot. (classic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

precursor to all sex steroids

A

cholesterol. 5 areas of substitutions to make the diff steroids (prog, androgens, CS, estrogen)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

steroid binding Rs parts and are where

A
  • nuclear. are TFs. turn on-off many genes

- steroid binding domain. area of dimerization. zinc finger (to bind DNA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

cells making testo

A

Leydig cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how to make DHT (dihydrotesto)

A

5 alpha reductase reduces the double bond of testo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

how to make estradiol

A

aromatase aromatizes double bond of testo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

pro hormone concept in steroid action

A

testo pro hormone. depending on tissue, will find testo OR a derivative (DHT, estradiol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

is estrogen a pro hormone (like testo)

A

no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

cell membrane steroid hormone Rs (SHRs) where and diff

A

allow faster response of transcription (1-5 min). nuclear SHRs = hours
*membrane SHRs in brain for sleep, etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

inhibin origin

A

testes Sertoli cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

inhibin fct

A

inhibit FSH release by gonadotropes of pit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

inhibin structure

A

Inhibin A: alpha + betaA subunits

Inhibin B: alpha + betaB subunits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

activin def

A

molecule made by combining 2x beta subunit of inhibin. either activin A, AB or B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

activin origin

A

gonadotropes and Sertoli cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

activin fct

A

regulate FSH secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

activin Rs are where

A

most of body tissues (just like androgens have Rs almost everywhere) effects not understood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

activin’s family of proteins

A

TGFbeta superfamily

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

testo Rs where in body

A

almost all tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

LH stim prod of hormones (like testo). testo (these hormones) effect in axis is what

A

feedback that is pulsatile (bc the LH release is pulsatile and therefore testo prod is pulsatile)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

gonadal vs periphery conc of testo

A

100x more in gonads. important concept for contraception and infertility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what cells make estradiol in the male

A

Leydig cells (same that makes testo)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

androgen (testo) and estradiol of Leydig cells fct in gonads

A

act on androgen Rs of Sertoli cells to promote germ cells dev

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

2 hormones of HPT axis secreted by Sertoli cells

A

inhibin and activin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

1 feedback in HPT axis for LH

A

-testo of Leydig cells feedbacks on gonadotropes in pulsatile fashion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

2 feedbacks in HPT axis for FSH

A
  • inhibin and activin of Sertoli cells act on gonadotropes

* note: makes sense bc FSH acts on Sertoli cells. (whereas LH acts on Leydig cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

inhibin feedbacks where in HPT axis

A

pituitary only (for FSH regul) (gonadotropes). not hypothalamus. bc doesn’t cross the BBB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

testo feedbacks where in HPT axis

A

both pituitary and hypothalamus (for LH regul)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

androgen disruptors def

A

chemicals that mimic androgens and disrupt the HPT axis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

LH vs FSH time of release by gonadotropes

A

same time (bc pulsatile GnRH acts at same time). but each has diff conc bc of diff half life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

interval of LH rise in the serum

A

60-90 min (same as GnRH pulsatility), bc after released, is degraded quickly (whereas FSH lasts long)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

interstitium of testes composition (between STs)

A

60% Leydig cells

macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

factors in how much steroid a Sertoli cell produces

A

size because bigger = more SER = more enzyme = more steroid produced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

LH R is where

A

cell membrane (Leydig)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

steps of LH signal to get testo prod in Leydig cell

A
  1. cholesterol in mt
  2. cholesterol side chain cleaved off
  3. pregnenolone released (dnm)
  4. 3 steps to make it into testo
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

rate limiting step in testo prod

A

cleavage of cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

how steroids (testo) are secreted out of the cell

A

via facilitated acid transport (bc are lipids)

it’s not like proteins and Ach, ntrs which use vesicles and packaging

49
Q

how testo gets to seminiferous tubules and into the circulation

A

bind high affinity proteins.

  1. TEBG (testosterone estradiole binding globulin) also called SHBG (sex hormone binding globulin)
  2. albumin
  3. ABP (androgen binding protein), in STs
50
Q

albumin binding capacity of steroids

A
  • low affinity

- huge capacity (bc lot of albumin)

51
Q

cells making ABP

A

Sertoli cells

52
Q

ABP gene

A

same as SHBG AND same protein backbone

53
Q

how ABP becomes diff from SHBG

A

difference in their liposilation

54
Q

2 peaks of testo before puberty

A
  • fetal (to become male)
  • neo-natal (after birth, mini puberty): to mark tissues as male. affects their protein and enzyme expression via epigenetics (methylation)
55
Q

testo constant or pulsatile secretion in the adult

A

pulsatile bc of pulsatile LH. + circadian rhythm with peaks in the morning

56
Q

testo variations in life after puberty

A

peak at 20, decreases after

57
Q

bound vs free testo

A
  • 2% free

- 98% bound (50% to SHBG, 50% to albumin)

58
Q

what testo is metabolically active

A

2% free + 49% bound to albumin bc easily picked up by tissues
(49% bound to SHBG is not bio active)

59
Q

liver disease consequence on free testo

A

increases. bc less SHBG (bc SHBG prod by liver)

60
Q

free vs bound DHT

A

highly bound (like testo)

61
Q

testo in males vs females

A

much higher in males

62
Q

estradiol in males vs females

A

same amount

63
Q

testo works where (androgen Rs are where)

A

all tissues. so androgen deficiency or excess = consequences everywhere

64
Q

steroid R affinity from lowest to highest

A
  1. cholesterol (milliM)
  2. progestins (nM)
  3. androgens (nM)
  4. estrogens (picoM)
65
Q

bisphinol A and AF def

A

chemicals working like estrogens bc stim the estrogen R

66
Q

2 estrogen Rs in male and female

A

alpha and beta

67
Q

alpha R of estrogen location

A

most tissues

68
Q

beta R of estrogen location

A

different from alpha R

69
Q

alpha vs beta R of estrogen

A

diff in their domains but same estrogen binding domain

70
Q

alpha vs beta R of estrogen difference

A
  • have the same affinity for certain substances but diff affinity for other substances
  • therefore, agonist + antagonist effect in diff parts of the body always diff (bc diff alpha to beta R affinity)
71
Q

effect of estrogen R alpha knockout in females

A

infertility

72
Q

effect of estrogen R alpha (ESR1) knockout in males

A
  • have spermatogonia and spermatocytes but no spermatids (DECREASED fertility)
  • back pressure atrophy (as if ligated the ductuli efferentes). estrogen in ED allows fluid resorption
73
Q

location of estrogen R alpha in males (ESR1)

A

efferent ducts (ductili efferentes)

74
Q

function of ESR1

A
  • regulates a gene in the efferent duct called CFTR (cystic fibrosis transporter receptor)
  • fluid absorption in ED
75
Q

mutation of CFTR consequence

A

infertility (no the CF mutation, don’t necessarily have CF)

76
Q

estrogen R alpha deficiency or aromatase deficiency in man consequence (aromatase makes testo into estradiol)

A
  • no closure of bone growth plate (very tall)
  • lower sperm motility
  • osteoporosis
  • normal sexual diff and pubertal maturation
77
Q

right word to describe the reduction in production of androgens in men with aging

A

Partial androgen deficiency in aging men (PADAM) (also called andropause)

78
Q

charact of andropause

A
  • decrease in testo and DHT as of 40+
  • increase in serum SHBG (less free testo)
  • decrease in testicular fct (spermatogenesis and steroidogenesis) with age. sperm quality decreases but count remains the same
  • decreased libido
  • decreased muscle strength
  • increasing risk of BPH (benign prostatic hyperplasia) and PC (prostate cancer)
79
Q

side effects of androgen deprivation (drop with age) (on tissues with androgen Rs)

A
  • bone loss (osteoporosis, fractures)
  • muscle weakness
  • hot flashes
  • loss of libido
  • erectile dysfunction
  • liver, skin, behavior effects
80
Q

drugs studied as hormone replacement therapy in men

A
  • testo
  • human growth hormone
  • DHEA
  • melatonin
81
Q

consequences of HRT in men

A
  • higher conc of RBCs (polycythemia)
  • CV effects
  • gynecomastia possible
82
Q

benefits of HRT in men

A
  • improved bone mass, muscle mass, strength
  • better physical fct
  • increased libido
83
Q

why can’t give testo as a pill

A

metabolized rapidly

84
Q

ways of administering testo

A
  • injection (male contraception)
  • patch
  • solution
  • roll-on
85
Q

when to give HRT in men (testo)

A

androgen deficiency (only**). only give to men with very low serum testo to bring them back to the lower end of normal range

86
Q

delay for male contraception to work and why

A

3 months. because fixed time of spermatogenesis in species. 64 days in man. have to wait for full cycle of spermatogenesis

87
Q

hormones essential to start spermatogenesis

A
  1. testo (high conc needed)

2. FSH (at puberty and re-initiation)

88
Q

hormones essential to maintain spermatogenesis

A

testo only

89
Q

most androgen sensitive step in spermatogenesis

A

the release of spermatids from the STs for spermiation (needs testo the most)

90
Q

effect of giving inhibin to an adult male on spermatogenesis

A

none because blocks FSH release but FSH not needed to maintain spermatogenesis

91
Q

knockout of FSH beta and FSH-R in animals consequence

A

fertile but smaller testes and less sperm

92
Q

minimal testo required to maintain spermatogenesis

A

third of normal gonadal amount

93
Q

spermatozoon charact

A
  • sheds all cytoplasm
  • haploid
  • repackages its chromatin
  • engine with mts
94
Q

what happens to sperm nuclei in spermatogenesis

A
  • histones removed (nucleosomes) (1. hyperacetylated to have less DNA affinity 2. transition prot pushes them out 3. RNA pushes transition prot).
  • replaced with small very basic protein (protamine). these cross-link during passage in the EDD***
  • methylation at same time. + maintain non coding RNAs, RNAs, acetyl and methyl sites
  • DNA more condensed
95
Q

info from sperm other than DNA delivered to the oocyte that is essential

A
  • RNAs (coding and non coding)
  • methylation sites
  • histones
96
Q

blood testis barrier formed by what

A

projections of Sertoli cells in ST epith

97
Q

proteins above vs below BTB

A

above: different and unknown to immune system
note: smart barrier that lets certain things through (active transport) but not Abs

98
Q

vasectomy effect on BTB

A

sperm leaks and get immune consequences on epith above BTB

99
Q

research being made for spermatogonial stem cell loss after chemo

A
  • in vitro spermatogenesis

- spermatogonial SC therapy

100
Q

where sperm matures

A

EDD

101
Q

something special of EDD

A

doesn’t divide and shed. never gets primary cancer

102
Q

cells in EDD

A
  • principal cc (abso and secrete)
  • halo cc (immune)
  • basal cc (protective, NOT stem cc)
  • apical (unknown fct)
  • clear cc (control pH in lumen)
  • myoid cc
  • interstitial SM cells and caps
103
Q

what takes up the cytoplasm of sperm in the seminiferous tubules + what is left

A

Sertoli cells

a cytoplasmic droplet remains

104
Q

what happens to the cytoplasmic droplet of spermatids

A

absorbed by clear cells of EDD + has many functions

105
Q

3 parts of EDD + ions variations

A
  • initial segment
  • caput
  • cauda
  • ions composition diff in all*
106
Q

why ion conc vary along the EDD

A

to maintain sperm in quiescent state

107
Q

what varies along the EDD other than ions conc

A

protein composition. so electrophoretic pattern changes. potential target for infertility or contraception

108
Q

what are exosomes (epididymosomes)

A

non coding RNAs secreted by principal cells of the EDD.

-enter nucleus of sperm and affect diabetic phenotype of the progeny

109
Q

how is paternal obesity reflected in the progeny

A

-through EPIGENETIC marks transferred in the sperm in epididymosomes
(NOT through the genome)

110
Q

how to properly dx infertility and why

A

3 semen samples taken at least 6 weeks apart

not 1 bc some people fluctuate and some constant values

111
Q

some sperm parameters

A
  • volume
  • total number
  • conc of sperm
  • motility
  • progressive motility
  • vitality
  • sperm morphology
112
Q

why the decrease in sperm prod in males in dev countries over last 50 years

A

because meiosis can’t take place at body temp (and we wear underwear, clothes, etc.)

113
Q

early erectile dysfunction linked with what

A

CV problems later in life

114
Q

other parameters for sperm quality

A

chromatin biomarkers

  • FISH for epigenetics, methylation, histones
  • non coding RNA
  • telomeres
115
Q

problem of lack of secretions in sperm, problem of sperm secretion indicates what

A

possible CF

116
Q

how sperm gets to the egg

A

-PGs produced by seminal vesicles + contraction of female reprod tract

117
Q

motility is only useful to sperm for what

A

drilling through proteins around the egg (fusion and adhesion to egg PM, ZP interaction, cumulus interaction)

118
Q

what happens to sperm mtDNA in the oocyte after fertilization

A

diluted

Bloc I - Reproduction (57 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions