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Endocrinology & Reproduction > Control of testicular function and sperm physiology > Flashcards

Control of testicular function and sperm physiology Flashcards

1
Q

main physiological function of the testes

A
  • production and release of testosterone

- spermatogenesis

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2
Q

what controls the functions of the testes

A

HPG-axis

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3
Q

hypothalamus role in HPG axis for testicular function

A

GnRH neurons

  • cell bodies in the preoptic acre of the H extend to the median eminence and release GnRH into the pituitary portal blood system
  • GnRH is released in regular pulses
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4
Q

how is GnRH released

A

regular pulses

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5
Q

where are GnRH neurons

A

in the hypothalamus, extend to the medien eminence

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6
Q

what releases GnRH

A

GnRH neurons in the preoptic acre of hypothalus

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7
Q

pituitary role in HPG axis for testicular function

A

release of LH and FSH from gonadotroph cells in the anterior pituitary in response to GnRH in regular pulses

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8
Q

what stimulates release of LH and FSH from gonadotrophs in anterior pituitary

A

GnRH

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9
Q

where is LH and FSH released from for testicular function

A

gonadotrophs in the anterior pituitary

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10
Q

how are LH and FSH released

A

regular pulses

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11
Q

GnRH stimulates the release of

A

FSH and LH

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12
Q

LH in males

A

stimulates production of testosterone in testes

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13
Q

FSH reproductive role in males

A

stimulates growth and maturation of the testes and spermatogenesis

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14
Q

why are testes located outside body

A

for optimum temperature of 35 degrees celsius

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15
Q

Anatomy of the testes

A

densley packed network of tubules feeding from testes to the epididymis to the vas deferens

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16
Q

what surrounds seminiferous tubulues

A

Leydig cells

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17
Q

where are leydig cells

A

surrounding the seminiferous tubulues

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18
Q

where does the epididymis lead to

A

vas deferens

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19
Q

what simulates the leydig cells

A

LH

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20
Q

what do leydig cells release

A

testosterone and other androgens

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21
Q

what effect does LH have on leydig cells

A

synthesis and release of testosterone and other androgens

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22
Q

main precursor of testosterone

A

pregnenolone

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23
Q

what is pregnenolone

A

precursor of testosterone

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24
Q

how is pregnenolone formed

A

conversion of cholesterol to pregnenolone by use of cholesterol desmolase, stimulated by LH

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25
Q

rate limiting step in formation of testosterone

A

cholesterol to pregnenolone, by cholesterol desmolase enzyme

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26
Q

enzyme for rate limiting step of testosterone formation

A

cholesterol desmolase

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27
Q

cholesterol desmolase

A

enzyme for rate limiting step of testosterone formation

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28
Q

effects of testosterone

A
  • male hormone
  • anabolic
  • development of primary and secondary sexual characteristics
  • libido & sexual behaviour
  • stimulates spermatogenesis
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29
Q

where does spermatogenesis occur

A

within the seminiferous tubulues

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30
Q

what do seminiferous tubules contains

A
  • spermatogonial stem cells

- sertoli cells

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31
Q

what do sertoli cells do

A

provide support, nutrition, protection and regulation for spermatogenesis

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32
Q

what cells provide support, nutrition, protection and regulation for spermatogenesis

A

sertoli cells

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33
Q

where are sertoli cells

A

seminiferous tubulues

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34
Q

what do spermatogonial stem cells produce

A

sperm

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35
Q

when does spermatogenesis begin

A

puberty

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36
Q

what are the divisions of spermatogenesis

A

mitosis followed by meiosis

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37
Q

rate of sperm production

A

120 million per day /// 1,500 per second

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38
Q

spermatocytogenesis

A

division of spermatogonial stem cells by mitosis to produce spermatocyte cells and replace themselves

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39
Q

DNA content of spermatogonial stem cells

A

diploid, 46

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40
Q

what division do spermatogonial stem cells under go

A

mitosis - to replace themselves and produce spermatocyte cells

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41
Q

how many subtypes of spermatogonial stem cells

A

3

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42
Q

what are the subtypes of spermatogonial stem cells

A

Type A dark
Type A pale
Type B

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43
Q

what do Type A dark spermatogonial stem cells do

A

replicate by mitosis to provide constant supply of type Ad and type Ap

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44
Q

what do Type A pale spermatogonial stem cells do

A

replicate by mitosis to provide type b cells

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45
Q

what do type b spermatogonial stem cells do

A

divide by mitosis into primary spermatocyte

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46
Q

dna content of primary spermatocyte

A

diploid

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47
Q

which spermatogonial stem cells divide to produce primary spermatocyte

A

Type B

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48
Q

spermatidogenesis

A

meiosis of primary spermatocytes to produce spermatids

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49
Q

dna content of spermatids

A

haploid, 23

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50
Q

what divides to produce spermatids

A

primary spermatocytes

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51
Q

spermiogenesis

A

4 phase process that converts symmetrical spermatids into mature sperm

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52
Q

4 phase process that converts symmetrical spermatids into mature sperm

A

spermiogenesis

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53
Q

4 phases of spermiogenesis

A
  • golgi phase
  • cap phase
  • acrosome phase
  • maturation phase
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54
Q

golgi phase

A
  • golgi apparatus creates vesicle of enzymes around nucleus on the side that is bound to the sertoli cell
  • mitochondria simultaneously moves to other side of the cell
  • centriole starts to form an axoneme
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55
Q

what is an axoneme

A

cytoskeletel core of the tail

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56
Q

Cap phase

A
  • spermatid DNA condensed in nucleus, excess removed
  • golgi surrounds nucleus and enzyme vesicle to form acrosomal cap
  • acrosomal cap covers front half of condensed nucelus surrounding sertoli cells
57
Q

what part of does acrosomal cap cover

A

acrosomal cap covers front half of condensed nucelus surrounding sertoli cells

58
Q

which stage forms the acrosomal cap

A

cap phase

59
Q

acrosome phase

A
  • axoneme extends into lumen of SFT to become tail

- temporary cytoskeleton called manchettes bind to nucles to support tail growth

60
Q

what are manchettes

A

temporary cytoskeleton that bind to nucleus to support tail growth of sperm

61
Q

maturation phase

A
  • excess cytoplasm is phagocytosed by sertoli to produce mature sperm
  • mitochondira move to central section of cell called middle piece
62
Q

where do mitochondria go in maturation of sperm

A

middle piece

63
Q

are mature sperm in SFT motile

A

no

64
Q

where do mature sperm gain motiltiy

A

in the epididymis

65
Q

where are mature sperm stored

A

epididymis

66
Q

what happens to sperm at epididymis

A

stored and gain motility

67
Q

what regulates sertoli cells

A

FSH

68
Q

functions of sertoli cells

A
  • form blood-teste barrier
  • release androgen binding protein
  • release inhibin for feedback on the pituitary
  • secrete supporting fluid into the lumen
  • phagocytose residual cyctoplasm from spermiogenesis
  • release range of proteins such as GDNF and AMH
69
Q

What forms the blood teste barrier

A

sertoli cells

70
Q

what releases androgen binding protein

A

sertoli cells

71
Q

what releases inhibin for feedback on the pituitary

A

sertoli cells

72
Q

what phagocytoses residual cytoplasm from spermiogenesis

A

sertoli cells

73
Q

where is the blood testi barrier

A

between blood and the seminiferous tubules

74
Q

how is blood testi barrier formed

A

tight junctions between sertoli cells form barrier between lumen of SFT and blood vessels

75
Q

purpose of blood teste barrier

A
  • allow sertoli cells to control lumen within the environment
  • protects developing sperm from toxins
  • separates sperm from autoimmune system
76
Q

why are sperm susceptible to toxins

A

bc they proliferate so rapidly

77
Q

why must sperm be seperated from the autoimmune system and how

A

because they are no longer recognised by the body, blood teste barries

78
Q

why is androgen binding protein released

A

spermatogenesis requires very high levels of testosterone around the developing sperm

79
Q

how does ABP maintain high levels of testosterone for spermatogenesis

A

binds to testosterone in th elumen making it less lipophillic so it cannot leave. this makes T concentrate in the lumen for increased fertililty

80
Q

what does the binding of ABP to testosterone stimulate

A

spermatogenesis

81
Q

what does testosterone suppress

A

LH secretion

82
Q

purpose of inhibin

A

produced by the sertoli cells to suppress FSH secretion by feedback on the pituitary

83
Q

prolactin in males

A

immune function, metabolism and male fertility

84
Q

how does prolactin effect male fertility

A
  • increases LH receptor expression on leydig cells
  • this increases testosterone release
  • increased T = increased spermatogenesis
85
Q

where is prolactin released in males for increasing fertility

A

pituitary

86
Q

what two systems work closely together to maintain male reproductivity

A

Leydig cells and seminiferous tubules

87
Q

stages of sperm transport to fertility

A

difficult journery

  • ejaculation
  • cervix
  • uterus & falloptin tubes
88
Q

ejaculation

A

deposition of sperm in the vagina

89
Q

cervix in sperm transport

A

mucuous barrier and crypts that act as sperm reservoirs, sperm motility is important

90
Q

uterus and fallopian tubes in sperm transport

A

mild contraction to propel the sperm towards th egg

91
Q

where does fetilisation occur

A

ampullary region of fallopian tube

92
Q

what happens in the ampullary region of the fallopian tube

A

fertilisation

93
Q

where does sperm capacitation occur

A

uterus

94
Q

what is sperm capacitation

A
  • chloesterol and glycoproteins are removed from the sperm cell surface by enzymes such as heparin
  • sperm is ‘switched on’ by calcium influx
95
Q

why are cholesterol and glycoproteins removed from sperm cell surface

A

they limit ion transfer on sperm cell surace

96
Q

how are cholesterol and glycoproteins removed from sperm cell surface

A

enzymes such as heparin

97
Q

what does heparin do

A

removed cholesterol and glycoproteins from sperm cell surface

98
Q

how does calcium influx effect sperm

A

upregulated ion transfer gives mitochondira burst of energy

99
Q

purpose of sperm capacitation

A

hyperactivity for increased motility

100
Q

acrosome reaction

A
  • interaction with ZP3 protein on the oocyte membrane prevents cross-species fertilisation
  • acrosome releases hyaluronidase and acrosin to break through egg coating to allow fertilisation
101
Q

what protein prevents cross species fertilisation and how

A

ZP3, extremely species specific

102
Q

where is ZP3

A

ooctye membrane

103
Q

what does ZP3 do

A

prevents cross species fertilisation

104
Q

what hydrolytic enzymes are released in the acrosome reaction

A

hyaluronidase and acrosin

105
Q

what type of enzymes are hyaluronidase and acrosin

A

hydrolytic

106
Q

purpose of hyaluronidase and acrosin

A

hydrolyse egg coating to allow fertilisation

107
Q

what triggers the acrosome reaction

A

sperm coming in contact with the oocyte

108
Q

ooctye activation

A

cortical granules are released and membrane becomes impermeable to other sperm
- male & female pronuclei is formed

109
Q

when is male and female pronuclei formed

A

ooctye activation

110
Q

when does oocyte activation occur

A

after fertilisation

111
Q

levels at which teste function can be distrubed

A
  • genetic
  • hypothalamic
  • pituitary
  • target tissue
112
Q

genetic distrubance of tests function

A

Klinefelter syndrome

113
Q

Klinefelter syndrome

A

disturbance of teste function at genetic level

114
Q

what is Klinefelter syndrome

A

male has XXY chromosome

115
Q

syndrom where male has XXY chromosome

A

Klinefelter syndrome

116
Q

possible effect of Klinefelter syndrome

A

hypogonadism and reduced fertility

range of effects, some wont show symptoms

117
Q

hypothalamic disturbance of testes function

A

Kallman syndrome

118
Q

Kallman syndrome

A

hypothalamic disturbance of teste function

119
Q

what is Kallman syndrome

A
  • when the GnRH neurones originate from the olfactory region of the brain and so don’t migrate to the hypothalamus
  • if olfactory mutated, GnRH neurones dont develop at all
120
Q

effects of Kallman sydrome

A

no reproductive functon and loss of smell cus of olfactory bulb dysfunction

121
Q

pituitary disturbance of testes function

A

hyperprolactinanaemia

122
Q

hyperprolactinanaemia

A

pituitary disturbance of teste function

123
Q

effects of hyperprolactinanaemia

A

abnormally high prolaction

- in high levels, prolactin inhibits GnRH

124
Q

what happens when there is too much prolactin

A

instead of upregualting GnRH, in large levels prolactin will inhibit GnRH

125
Q

what causes hyperprolactinanaemia

A

pituitary tumours

most commonly a side effect of presciprtion drugs that affect dopamine

126
Q

side effects of hyperprolactinanaemia in males

A

decreased libido and reduced fertilty

127
Q

target tissue level disturbances of teste function

A

androgen insensitivity syndrome

128
Q

androgen insensitivity syndrome

A

target tissue level disturbances of teste function

129
Q

what causes androgen insensitivity syndrome

A

genetic defects in androgen receptors that reduce sensitivty to testosterone and other androgens

130
Q

symptoms of androgen insensitivity syndrome

A

varies, depending on level of insensitivity

males can develop uterus or uterus and testes, but will still be genetically male

131
Q

what causes devlopment of internal female genitalia in males

A

complete androgen insensitivity casuing hyperandrogemia

132
Q

complete androgen insensitivity

A

zero response to testosterone and so female internal genetalia devlop despite XY chromosomes

133
Q

why is a male contraceptive pill difficult?

A

sperm have high proliferation rate, compared to females who produce one egg

134
Q

what are the current effects of a male contraceptive pill

A

they can reduce rate of sperm proliferation, but not switch off

135
Q

effect of steroids on male fertility

A

anabolic steroids like testosterone reduce fertility by supressing HPG axis through nagative feedback which switches off LH production

136
Q

how do anabolic steroid reduce male fertility

A

by supressing HPG axis through nagative feedback which switches off LH production

137
Q

non hormonal factors that effect sperm production

A
  • environment
  • climate
  • radiation (?)
  • air pollutio
  • food chain pollution
  • stress
138
Q

how do non-hormaon factors effect sperm

A

they increase oxidative stress leading to sperm damage

139
Q

what does oxidative stess do to sperm

A 
causes:
- protein damage
- lipid peroxidation
- biommembrane damage
- dna damage
= sperm damage

Endocrinology & Reproduction (15 decks)

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