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Sem4 REPRO > Basics of Reproduction > Flashcards

Basics of Reproduction Flashcards

1
Q

what is sexual differentiation?

A

formation of the male internal and external genitalia

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2
Q

what is genotypic/embryological sex?

A

based on presence of XX or XY chromasome

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3
Q

what is gonadal sex?

A

presence of ovaries or tester

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4
Q

what is phenotypic sex?

A

based on internal and external genitalia

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5
Q

what is legal sex?

A

the sex which is placed on birth certificate/ passport etc.

implicated in sports, marriage, hereditary - prince/princess

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6
Q

what is gender identity?

A

gender based on how a person feels - their perceived gender

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7
Q

how is gonadal sex determined?

A

XY chromosome causes SRY to be expressed on Y chromasome –> acts as a transcription factor –> causes formation of the testes NOT ovaries

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8
Q

what is SRY?

A

Sex determining region Y

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9
Q

at what point is SRY expressed?

A

week 7

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10
Q

other than testicular development, what effect does SRY have?

A

Sertoli Cell production – forms AMH - mullarian duct regression

Leydig Cell production - produces testosterone - causes internal genitalia formation - epididymis, vas defferens, seminal vesicle and prostate

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11
Q

at what point do the genital ridges change from bipotential to specific - why?

A

bipotential - mullarian and wolffian ducts present

week 7 - expression of SRY leads to sertoli cell formation – AMH causes regression of the malarian duct and the Wollfian duct remains patent.

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12
Q

where does the genital ridge arise from?

A

primordial mesenchymal germ cells

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13
Q

what is the role of primitive sex cords in the genital ridge?

A

run ontop of the genital ridge - migrate along
in the male - migrate in a long thin wave - become the Sertoli cells secreting AMH
in the female - migrate in bursts - form the granulosa/follicular cells - secrete oestrogen

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14
Q

what is the role of 5 alpha reductase/

A

conversion of testosterone to DHT in the genital skin

DHT acts as a potent androgen causing differnetiatiion of the male external genitalia

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15
Q

how does the male external genitalia develop?

A

genital tubercle develops into the glans penis
labia fuse and become rugged into the scrotum
prostate formation
urethral plate expands and rolls over to become the penile urethral fold

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16
Q

how do the female external genitalia develop?

A

in the absence of DHT, the labia, vagina and clitoris remain patent

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17
Q

what happens when testosterone is converted to oestrogen - what effect can this have?

A

oestrogen and other steroid hormones used in the development of the CNS - become the cortex, limbic system and spinal cord

excessive sex hormone can lead to people ‘feeling’ the wrong sex - there is a change in nuclear neuronal size

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18
Q

what is gonadal dysgenisis - what is an example of this condition?

A

when sexual differentiation is incomplete - usually due to a lack of SRY in males, or only one X chromosome in females

Turners Syndrome

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19
Q

what are the symptoms of Turners Syndrome?

A

there is a lack of testes due to no SRY
but there is ovarian dysgenisis due to only one X chromosome –> failure of function
there is a lack of DHT so uterus and tube form - they are small due to a defect in growth and development

20
Q

is it possible for people with turners syndrome to be fertile?

A

yes if they have a mosaic mutation for the disease

21
Q

what is sex reversal?

A

when the phenotype does not match the genotype

22
Q

what is intersex? what condition does this occur in

A

when there is components of both tracts - e.g. a uterus with testes

Androgen insensitivity syndrome

23
Q

what is AIS - what is the presentation?

A

XY individual
testosterone is produced but does not have an effect- e.g. receptor mutation, defect in second messengers

normal teste formation due to SRY
female external genitalia due to absence of testosterones action

24
Q

what are the two types of AIS?

A

complete = undescended testes, appear female at birth

partial = SOME modulation of the receptor - varying degrees of penile and scrotal development
- can start with female gentialia and then develop penis and testes at puberty

25
Q

what are the factors for diagnosis of AIS?

A 
primary amennhorea
lack of body hair
undescended testes
karyotype of male
male levels of androgens
26
Q

how is AIS treated?

A

see what the patient decides based on their gender identity

surgery

27
Q

what is the effect of a 5 alpha reductase deficiency

A

testosterone is present but no DHT
due to a mutation in the enzyme
normal production of the testes using SRY
differentiation and growth of the wolfing duct structures due to the presence of testosterone
NO MALE EXTERNAL GENITALIA
sudden increase in testosterone at puberty can cause virrilisation

may feel male even if female

28
Q

what is the inheritance pattern for 5 alpha reductase deficiency?

A

autosomal recessive

29
Q

How does CAH occur? explain using the steroid pathway?

A

steroids formed from cholesterol
cholesterol taken into cells and modified through the steroid pathway
side chain cleavage enzymes forms a 21C progesterone skeleton
progesterone converted to cortisol in the adrenal cortex by 21-hydroylase

DEFICENCY OF 21-HYDROXASE IN CAH

so there is a build up of progesterone
excess progesterone shunted into androgen pathway forming testosterone
very small amount of testosterone converted to oestrogen

low levels of cortisol feeds to the hypothalamus causing CRH release
CRH release causes ACTRH release from pituitary
ACTH causes uptake of cholesterol into the adrenal cortex
upregulates cholesterol levels to try to increase cortisol
unsucsessful due to deficiency - leads to further increase in testosterone

30
Q

what effect does high levels of androgens due to CAH have?

A

coffin ducts do not regress - so seminal vesicles and vas deferens form
mullarian ducts are present due to no AMH - so there is formation of the uterus, uterine tubes and upper 1/3rd vagina
ovaries present
DHT levels are high - so there is formation of male external genitalia

lack of aldosterone means there is no water regulation - so causes salt wasting
– treat with glucocorticoids.

31
Q

what is behavioural sex?

A

the exposure or lack of exposure of the brain to testosterone during development - effects:
= sexual beahviours
= sexual orientation
= increased aggression
= increased rough and tumble play in the prepubertal stage

32
Q

what is the role of the HPG?

A

control of reproduction through MAINLY negative feedback

33
Q

what is the pathway which controls the release of oestrogen, progesterone and testosterone from the gonads?

A

kisspeptin –> activates hypothalamus –> GnRH release to anterior pituitary –> LH and FSH release from anterior pituitary –> gonads

34
Q

how does GnRH reach the anterior pituitary to produce an effect?

A

via the primary plexus - binds to gonadotroph cells the produce LH or FSH

35
Q

what is the difference between the structures of gonadal hormones?

A

common alpha subunit
differing hormone specific beta subunit
differing glycosilation patterns to match the specific receptors

36
Q

how is GnRH released in pulses? what is the relevance to this?

A

using a pulse generator to maintain frequency and amplitude

slow pulse frequency causes FSH release
fast pulse frequency causes LH release

pulses vital for maintaining control of the menstrual cycle

37
Q

what is the time frame for GnRH release?

A

30-120 mins in females- depending on stage in the menstrual cycle
90-120 mins in male

38
Q

what type of hormone is GnRH?

A

small decapeptide- cleaved from a large preprohormone

39
Q

how are gonadotrophin hormones released?

A

pulsatile due to gnRH release - although not vital to function

40
Q

what is the role of LH?

A

stimulates leydig cells to produce testosterone
stimulates theca cells to produce androgens
stimulates ovulation and production of corpus luteum

41
Q

what is the role of FSH?

A

control of sertoli cells and spermatogenesis

control of the follicle and granulosa cells - formation of oestrogen from the theca androgens

42
Q

what happens if there is defect in the LH receptor?

A

there is no ovulation

so the person is infertile

43
Q

what is the role of synthetic GnRH?

A

stimulation of the HPG

44
Q

what is the role of GnRH analogues?

A

inhibition of the HPG

agonists - cause decoupling of GnRHr from the G-protine second messenger over a few weeks

antagonists - bind to the GnRH receptor and stops binding

45
Q

when might GnRH analogues be used?

A

PCOS endometritis
IVF - prevents FSH and LH release - can then be given exogenous forms to control menstrual cycle
prostate and breast cancer which are hormone specific
gondal protection before chemotherapy - stops the DNA from being damages

Sem4 REPRO (17 decks)

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