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SEM4 > Intro repro > Flashcards

Intro repro Flashcards

1
Q

Sexual determination

A

genetically controlled process dependent on ‘switch’ on Y chromosome – chromosomal determination of male/female

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2
Q

Sexual differentiation:

A

internal + external genitalia develop as male/female process

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3
Q

Where is SRY gene

A

sex determining region on Y chromosome

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4
Q

SRY gene

A

switches ON week 7 so gonad –> testis

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5
Q

What cells does testis develop

A

Sertoli cells

Leydig cells

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6
Q

Sertoli cells

A

produce AMH

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7
Q

Leydig cells

A

produce testosterone

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8
Q

AMH

A

Anti Mullerian Hormone

inhibits Mullerian ducts, via apoptosis of Mullerian ducts – regresses

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9
Q

Gonad precursors

A

Mesenchymal tissue

Genital ridge

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10
Q

Where genital ridge

A

posterior thoracic-lumbar region

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11
Q

Mullerian duct

A
  • females - to produce internal female organs
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12
Q

Wolffian ducts

A
  • males - to produce internal male organs
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13
Q

Cell types which invade into genital ridge forming gonad?

A
  1. Primordial cells -
  2. Primitive sex cords
  3. Mesonephric cells
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14
Q

Primordial cells male/female

A

precursors of gametes
male = spermatogonia/spermatozoa
female = oogonia

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15
Q

Primitive sex cords male/female

A

form
male = Sertoli cells - SRY + AMH
female = granulosa cells

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16
Q

Mesonephric cells

A

form
male = leydig
female = theca cells

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17
Q

Describe route of primordial cells

A
  • in clusters in yolk sac’s epithelial

- week 3 divide via mitosis + migrate via connective tissue of hind gut to genital ridge

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18
Q

Describe route of primitive sex cords

A
  • on epithelium that overlie genital ridge
  • primordial cells colonise ridge
  • migrate into ridge in columns
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19
Q

Male sexual determination? (Step by step)

A
  1. SRY is present due to the presence of the Y chromosome
  2. Sex cords penetrate deep into mesenchyme
  3. Surround primordial cells forming testis cord
  4. Turn into sertoli cells - release AMH degenerating mullerian ducts
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20
Q

Female sexual determination? (Step by step)

A
  1. No Y chromosome
  2. Sex cords ill-defined
  3. Don’t penetrate deeply into mesenchyme
  4. Condense into cortex as small clusters surrounding primordial cells
  5. Form granulosa cells
  6. Absense of androgens dengerates Wolffian ducts
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21
Q

Origin of mesonephric cells

A

Originate from Mesonephric primordium lateral to genital ridge

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22
Q

Describe route of mesonephric cells

A

-some mesonephric cells migrate to genital ridge
-act as “Androgen secreting cells”
Males - under influence of pre-sertoli cells forming testosterone
Females - vascular tissues - Theca cells synthesises androgens

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23
Q

internal male

A
  1. Vas deferens
  2. Seminal vesicles
  3. Prostate
  4. Epididymis
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24
Q

internal female

A
  1. 1/3 top of the vagina
  2. Fallopian tubes
  3. Cervix
  4. Uterus
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25
Q

Male sexual differentiation? (Step by step)

A
  1. Gonads develop at genital ridge level in thoraco-lumbar region
  2. Testerone + AMH (from sertoli + leydig cells) degenerate Mullerian ducts
  3. Wollfian duct develops - Seminal vesicles, prostate, epididymis, vas deferens
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26
Q

Female sexual differentiation? (Step by step)

A
  1. Gonads develop into ovaries
  2. No AMH + testosterone, mullerian ducts grow - uterus, uterine tubes, cervix, upper 1/3rd of vagina
  3. Wollfian ducts regress
27
Q

Dihydrotestosterone (DHT)

A

Hormone for male external genitalia

  1. Clitoral area –> penis
  2. Labia fuses + ruggated –> scrotum
  3. Prostate forms
28
Q

Where’s 5 α-reductase

A

genital skin

29
Q

5 α-reductase

A

Adds a hydrogen molecule to testosterone –> POTENT DHT

30
Q

Identical features male/female before differentiation

A
  1. Urethral fold
  2. Genital swelling
  3. Genital tubercle
31
Q

How does the presence of DHT affect the genital tubercle?

A

phallus of the penis

32
Q

How does the presence of DHT affect the urethral ford?

A

Folds together forming hallow tube –> shaft of penis.

33
Q

What happens to the genital swelling in the absence of DHT?

A

forms labia majora + minora

34
Q

What happens to the urethral fold in the absence of DHT?

A

forms vaginal opening

35
Q

What happens to the genital tubercle in the absence of DHT?

A

forms clitoris

36
Q

Gonadal dysgenesis

A

incomplete sexual differentiation, missing SRY in male or partial/complete deletion of 2nd X in female – describes abnormal development of gonads

37
Q

Sex reversal:

A

phenotype doesn’t match genotype

38
Q

Intersex

A

have components of both tracts or ambiguous genitalia – sex of infant difficult to determine

39
Q

Cause of AIS (Androgen Insensitivity Syndrome)?

A

Testosterone production via sertoli cells BUT undetected due to:
Mutated testosterone receptor
Error in signalling pathway

40
Q

AIS presentation

A
  • Genotypically male but female external genitalia.
  • No male or female internal genitalia
  • Has testis within abdominal cavity
41
Q

Why do AIS patients have no male or female internal genitalia?

A
  • Y chromosome
  • SRY proteins expressed
  • gonad –> testis
  • sertoli cells from primitive sex cords
  • AMH degenerates mullerian ducts so NO internal female genitalia
  • leydig cells produce testosterone but undetected so Wolffian duct regresses
42
Q

Why do AIS patients have a female external genitalia?

A
  • 5-a-reductase in genital skin convert testosterone into DHT
  • DHT also binds to testosterone receptors
  • no response
  • no external male genitalia
43
Q

Diagnosis of AIS

A
  • Amenorrhoea
  • High levels of testosterone
  • Lack of hair
  • Ultrasound will show testis within the body
  • Karyotyping - Will show XY rather than XX
44
Q

5-a-reductase deficiency

A

Testosterone made, acts on body but lack 5-a-reductase SO NO DHT produced

45
Q

What happens in 5-a-reductase deficiency?

A
  1. Y chromosome so SRY
  2. Forms Testis, sertoli cells, Leydig cells
  3. Testis + leydig cells form testosterone
  4. Forms internal male genitalia from Wollfian ducts.
  5. Sertoli cells produce AMH degenerating Mullerian ducts so female internal genitalia not made
  6. Testosterone wants to get converted into DHT via 5-a-reductase BUT lack so lack development of male external genitalia.
46
Q

why does 5-a-reductase deficiency differ?

A

Some people may continue to develop male external genitalia once puberty as HIGH testosterone so HIGH substrate which may tip the development to correct side (more substrate = more product even if the reaction is slower due to a decreased amount in the enzyme)

47
Q

Presentation of Turner’s

A
  1. no Y chromosome
  2. no SRY
  3. produce Ovaries
  4. no AMH so Mullerian ducts continue growing
  5. Testosterone levels wouldn’t be high so Wollfian ducts regress.
  6. internal + external female genitalia.
48
Q

Complications in turner syndrome patients

A
  1. Failed ovarian function - due to only 1 X chromosome
  2. Streak ovaries - ovarian dysgenesis (both chromosomes required for normal development of ovaries)
  3. Uterus + uterine tubes - small but present
  4. Growth + puberty problems
  5. Infertility (mocaicisim - increases the chances of fertility)
49
Q

treatment Turner’s

A

Hormone support - for bones and the uterus

50
Q

CAH (Congenital Adrenal Hyperplasia) cause?

A

No cortisol production due to lack of 21-hydroxylase.

51
Q

CAH (Congenital Adrenal Hyperplasia) problem of HPA axis

A
  • lack of 21-hydroxylase
  • no cortisol
  • no negative feedback inhibiting continuous production of CRH +ACTH
  • build up of androgens in adrenal cortex as desired cortisol/aldosterone not be produced.
52
Q

Presentation CAH

A
  1. XX no SRY
  2. Gonads –> ovaries
  3. Lack sertoli cells = no AMH so mullerian cells develops female internal genitalia
  4. Lack leydig cells = no testosterone from them via defective 21-hydroxylase BUT rather than cortisol being produced, androgens including testosterone is produced.
  5. testosterone –> internal male genitalia from Wollfian ducts.
  6. Testosterone –> DHT –> external male genitalia even if genotype XX
53
Q

Complications of CAH

A
  • various degree of enzyme block which is specific to each individual patient
  • No aldosterone so lethal salt wasting
54
Q

CAH treatment

A

Treated with glucocorticoids (cortisol) to correct feedback.

Exogenous cortisol return negative feedback + present salt wasting.

55
Q

AIS genotype + internal/external genitalia

A

XY
internal = female
external = female

56
Q

5-a-reductase deficiency genotype + internal/external genitalia

A

XY
internal = make
external = female

57
Q

Turner’s genotype + internal/external genitalia

A

XO
internal = female
external = female

58
Q

CAH genotype + internal/external genitalia

A

XX
internal = male + female
external = male

59
Q

How does oestrogen and oestradiol differ?

A

Oestradiol has varying numbers of -OH groups

60
Q

Why does the adrenal cortex produce sex hormones?

A

All the cholesterol-based hormones are made in a chain reaction to produce cortisol + aldosterone, adrenal cortex first produces sex hormones.

61
Q

21-hydroxylase

A

form aldosterone + cortisol

62
Q

Hypothalamic-pituitary-adrenal axis

A
  • hyprothalamus releases CRH (corticotropin releasing hormone)
  • stimulates cells in A.pituitary
  • release ACTH (adrenocorticotropic hormones)
  • work on adrenal cortex to produce cortisol.
  • system runs on negative feedback.
63
Q

ACTH

A
  1. Increasing uptake of cholesterol in adrenal cortex
  2. Upregulating expression of the cholesterol cleaving enzymes - p450 enzymes
  3. secretion of glucocorticoids decrease.

SEM4 (6 decks)

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