Embryology-Male Sexual Differentiation Flashcards

1
Q

What are the different factors that contribute to one’ sex?

A

Chromosomal sex, gonadal sex, phenotypic sex

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2
Q

When does sexual differentiation begin in utero?

A

6-7 weeks

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3
Q

What is the consequence of differentiation of the hypothalamus?

A

The male hypothalamus is no longer able to produce the LH surge necessary for ovulation in females.

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4
Q

What area of the brain has remarkable changes in response to steroids in puberty?

A

Hypothalamus. The set point for steroid hormone feedback becomes markedly elevated.

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5
Q

Where do the gonads come from?

A

4-5 wks: genital ridge forms -> Germ cells migrate from yolk sac to genital ridge -> genital ridge seeded w/germ cells

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6
Q

What determines how many eggs a woman will have for the duration of her life?

A

The number of germ cells that populate the ovaries during gestation.

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7
Q

What ductal systems are associated with the seeding of the gonadal ridge?

A

Wolffian (mesonephric) duct and Mullerian (paramesonephric) duct. These will develop into the internal sex structures (Wolffian for males and Mullerian for females)

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8
Q

What triggers the differentiation of the gonad into testis?

A

Y chromosome codes for testis-specific proteins and hormones (testosterone & Mullerian inhibiting hormone) that will transform the gonad into a primitive testis. This all happens around 6-7 weeks.

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9
Q

Which sex is the differentiation by default?

A

Female: males need testosterone and Mullerian inhibiting hormone to develop male characteristics.

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10
Q

What is the function of Mullerian duct inhibiting factor made by sertoli cells?

A

Mullerian duct regression, eliminates structures that would become the uterus and fallopian tubes

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11
Q

Drivers for male sexual differentiation

A

Mullerian inhibiting factor and testosterone

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12
Q

What tells the Leydig cells to make testosterone?

A

Not the mother’s or the fetal’s hypothalamus, hCG from the placenta is the fetal “LH”.

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13
Q

What structures are dependent on testosterone for development

A

Wolffian duct (epididymus, vas deferens, seminal vesicles and ejaculatory duct). The urogenital primordia (penis, corpus spongiosum, scrotum, prostate and bulbourethral gland) are all dependent on testosterone conversion to DHT by 5-alpha-reductase.

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14
Q

Why is 5-alpha-reductase essential for almost all tissues in males?

A

All tissues aside from the Wolffian duct will only react to DHT. Without 5-alpha-reductase testosterone is inactive.

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15
Q

Where do men get their estrogen?

A

Testis

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16
Q

Does a person with complete testicular feminization have testicles or ovaries? What is their level of testosterone in the blood?

A

Testis. Testosterone is high, they are feminized because they are deficient in 5-alpha-reductase. In the absence of testosterone the wolffian ducts regress, urogenital folds develop into a clitoris, labia and lower vagina. Since there is still mullerian inhibition substance the oviduct, uterus and upper vagina do not develop.

17
Q

What contributes to the spectrum of differentiation of male to female in testicular feminization?

A

Inactive mullerian inhibiting substance allows for differentiation of mullerian ducts (oviduct, uterus and upper vagina). Ranges in 5-alpha-reductase is also a big player.

18
Q

Where can women get androgens to masculinize?

A

Hidden testis, adrenal gland and drug store.

19
Q

Ambigous female genitalia due to adrenal problems?

A

Congenital adrenal hyperplasia -> 21-hyrdoxylase deficiency pushes all steroid hormone precursors towards androgen biosynthesis.

20
Q

Why don’t girls develop breasts earlier in life?

A

They hypothalamic set point (cycling center) is very sensitive to feedback inhibition by estrogen and progesterone. At puberty the hypothalamic set point shifts way up and it takes way more estrogen and progesterone to inhibit the hypothalamus. Consequently levels of GnRH go way up and LH/FSH secretion increases. The ovary begins to produce lots of estrogen and progesterone. Males are similar, but with testosterone instead of estrogen and progesterone.

21
Q

What hormone is responsible for breast development during puberty?

A

Ovarian estrogen

22
Q

What drives expression of pubic and axillary hair?

A

Adrenal androgens

23
Q

What are sources of precocious puberty?

A

Adrenal (up regulation of estrogen/testosterone), central (increase in hypothalamic set point to negative feedback), idiopathic or space occupying lesion near the hypothalamus.

24
Q

What single hormone would you measure to make a diagnosis of central precocious puberty vs. peripheral precocious puberty.

A

LH. Normal rules out precocious puberty. High = centrally mediated. Low = peripherally mediated.

25
Q

Causes of central precocious puberty?

A

Tumors near hypothalamus, CNS injury caused by inflammation, surgery, trauma or radiation and congenital abnormalities (hydrocephalus, cysts)

26
Q

How do you treat central precocious puberty?

A

GnRH analogue therapy (leuprolide). Pummeling a GnRH receptor with tons of GnRH analogue causes the pituitary to regress all of its GnRH receptors and it won’t put out any gonadotropins at all.

27
Q

How do you treat peripheral precocious puberty?

A

Treat the underlying condition.

28
Q

Why do kids with precocious puberty start as the biggest kids in the class and end as the smallest kid in the class?

A

Their epiphyseal plates close faster despite accelerated growth in the beginning.

29
Q

Endocrine disruptors in the diet that may account for the increasing earlier age in the onset of puberty?

A

Chemicals that can be converted to active steroids by our tissues: insecticides, herbicides, fungicides, plasticizers, cosmetics and detergents.