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Phys II Unit III > 3 Puberty > Flashcards

3 Puberty Flashcards

1
Q

What are the three levels of sexual differentiation?

A

Genetic sex (depends on the combo of sex chromosomes at the time of conception)

Gonadal sex (whether testes or ovaries develop - determined by presence or absence of Y chromosome)

Phenotypic sex (apparent anatomic sex of individual, usually determined by gonadal sex)

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2
Q

What genetic determinant promotes testis differentiation?

A

Sex-determining Region of the Y chromosome (SRY)

Makes Testis Determining Factor (TDF)

Females lack SRY gene, therefore their gonads do not receive a signal for testicular development

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3
Q

Can you develop ovaries if you only have one X chromosome?

A

No. Two X chromosomes are required for the active genetic pathways necessary for ovarian development

XO (Turner’s syndrome) —> ovarian dysgenesis

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4
Q

During the first ________ of gestational life, gonads are indifferent or bipotential

A

5 weeks

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5
Q

In genetic males, the ______ gene of the ____ chromosome produces ______ which influences gonadal development into testis during gestational weeks _____.

A

SRY gene
Y chromosome
TDF
Weeks 6-7

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6
Q

If TDF does not initiate the development of testes, female gonads (ovaries) begin to develop at what gestational age?

A

Week 9

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7
Q

Testes develop with what three cell types?

A

Germ cells (spermatogonia)

Sertoli cells (produce anti-Müllerian factor)

Leydig cells (produce testosterone)

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8
Q

Ovaries develop with what three cell types?

A

Germ cells (oogonia)

Granulosa cells (produce estradiol)

Theca cells (produce androgens and progesterone)

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9
Q

________ differentiate into male reproductive tract and _______ differentiate into female reproductive tract

A

Wolffian ducts —> male

Müllerian ducts —> female

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10
Q

As testes develop, they secrete _________ from Sertoli cells and _________ from Leydig cells

A

Anti-Müllerian hormone from Sertoli cells

Testosterone from Leydig cells

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11
Q

________ promotes differentiation of the Wolffian ducts into the internal genitalia —> epididymis, vas deferens, seminal vesicles, and ejaculatory ducts

A

Testosterone

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12
Q

________ causes atrophy of the Müllerian ducts, which would have become the female genital tract if they were not suppressed

A

Anti-Müllerian Hormone

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13
Q

____________ stimulates the differentiation of the external genitalia around gestational week ________.

A

Dihydrotestosterone (DHT), a testosterone derivative from 5a-reductase

Week 9-10

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14
Q

Without DHT, _________ external genitalia develop

A

Female-like

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15
Q

Are hormones needed to cause the development of the female gonads?

A

No HORMONES are needed, but development does require two functional X chromosomes

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16
Q

In females, the _________ do not regress, giving rise to the ________, _______, and _________.

A

Anti-Müllerian ducts —> Fallopian tubes, uterus, and upper 1/3 of vagina

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17
Q

If a gonadal female is exposed to high levels of androgens in utero, the external genitalia will …

A

Differentiate into a male-like phenotype

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18
Q

If a fetus lacks the 21-hydroxylase enzyme, what will happen?

A

21-hydroxylase is involved in the biosynthesis of aldosterone and cortisol

Lack of cortisol production —> excessive ACTH —> hyperplasia of adrenal cortex and excessive adrenal androgens

In XX fetuses, ovaries and internal genitalia develop but external genitalia will VIRILIZE —> enlarged clitoris, labial folds appear as an empty scrotum

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19
Q

Most common cause of genital ambiguity

A

21-hydroxylase deficiency

Can lead to life-threatening adrenal insufficiency within the first weeks of life

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20
Q

What’s another name for 21-hydroxylase deficiency?

A

Congenital adrenal hyperplasia

Acne, clitoromegaly, and hirsutism due to adrenal or gonadal androgen excess

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21
Q

How do XY individuals lacking SRY gene develop?

A

Develop as female but NO GONADS

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22
Q

How do XX individuals with SRY translocation develop?

A

Develop as male, with testes

Would only known they are XX if you did chromosomal analysis

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23
Q

How do XY individuals with defective AMH production or action develop?

A

Would develop with male external genitalia, but both male and female internal organs, and testes for gonads

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24
Q

How would an XY individual with an absence of testosterone production or action develop?

A

Female-like external genitalia, but no male or female internal tracts, just testes

Usually a lack of receptors (insensitive to testosterone)

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25
Q

How would an individual with 5a-reductase deficiency develop?

A

Would have testes, male internal genitalia but female-like external genitalia (male pseudohemaphrotidism)

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26
Q

What would lab findings look like if you had a patient with suspected complete androgen insensitivity syndrome?

A 
Testosterone: high-normal
DHT: normal
FSH and Inhibin: normal
LH: high
AMH: high
Chromosome karyotype: 46XY
U/S: no ovaries, no uterus, male testes
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27
Q

What is the treatment for complete androgen insensitivity syndrome?

A

Laparoscopic gonadectomy followed by estrogen replacement therapy

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28
Q

How is complete androgen insensitivity syndrome diagnosed?

A

In infancy, due to inguinal masses (undescended testes with nowhere to go)

If not infancy, they typically get classified as female at birth and are diagnosed at puberty because of primary amenorrhea

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29
Q

When does puberty typically begin?

A

8-13 years for girls

9-14 years for boys

30
Q

What are the main characteristics of puberty?

A

Maturation of the hypothalamic-pituitary-gonadal axis —> appearance of secondary sex characteristics, acceleration of growth, and capacity for fertilization

31
Q

Start of puberty in males is marked by …

A

Increase in testicular size (gonadarche), followed by development of pubic hair and penile enlargement, as well as increased muscle mass

32
Q

Sperm production and ejaculatory capability are developed in males around ______ years old

A

13.5 - 13.7 years

33
Q

Adult testicular volume and penile size are achieved by ________

A

16 years of age

34
Q

Final height in males is reached by _______.

A

18 years of age

35
Q

Start of puberty in females is marked by _________.

A

Thelarche (breast development), at 10.9 years on average

36
Q

Typical course of female puberty

A

Thelarche at ~10.9 —> Pubarche at ~11.2 —> Menarche, usually by 13th birthday

37
Q

The first few menstrual periods for girls are ________, because _______

A

Non-ovulatory

No positive feedback by estrogen

38
Q

What happens to a girl’s body shape as puberty progresses?

A

Adipose tissue deposited around the hips

Hips enlarge and pelvic inlet widens

39
Q

What hormones are most important in the pubertal growth spurt?

A

GH and IGF-1

40
Q

In girls, growth spurt begins in ________ and is complete by _________

A

Early puberty

Menarche

41
Q

In boys, growth spurt begins near ________, almost _______ later than girls

A

Near the end of puberty

2 years later

42
Q

What happens to body composition during puberty?

A

Men develop 1.5x higher lean body mass, skeletal mass, and muscle mass than women

Women develop twice as much fat

43
Q

_____ functions to fuse epiphyses towards the end of puberty in both males and females

A

Estrogens

High levels of estrogen —> shorter stature

The longer time to reach puberty in boys accounts for most of the difference in stature

44
Q

Other things that happen during puberty

A

Bone density increases

Periodontal disease may appear (mouth flora changes)

Acne appears (testosterone-induced sebaceous gland activity)

45
Q

What is responsible for pubertal timing?

A

Reactivation of gonadotropin synthesis and secretion
• Hypothalamic Maturation Hypothesis - reduction in intrinsic suppression of GnRH
• Gonadostat Hypothesis - decreased sensitivity to the negative feedback of estrogen or testosterone

INCREASE IN PULSATILE GnRH RELEASE - first occurs during sleep —> increased ratio of LH/FSH release in both sexes that correlates with teh onset of puberty (reverses in late puberty)

46
Q

What is the major determinant in the timing of puberty?

A

Genetics

47
Q

What are some other factors that influence timing of puberty?

A

Geographic location
Exposure to light
Psychological factors
General health and nutrition

48
Q

More important than weight in the timing of puberty is ….

A

Percentage of body fat - from 16-23.5%

49
Q

What is the Leptin theory for the timing of puberty?

A

Puberty is physiologically gated by the energy resources of the body

Delayed puberty in female ballet dancers and accelerated puberty in obese females

A metabolic signal from adipose tissue may control onset of sexual maturation

Leptin, a protein produce of the obese gene secreted as a hormone from adipose tissue

50
Q

What is the function of Leptin?

A

Plays an important role in the regulation of body weight and metabolism

Plasma levels are correlated with the degree of adiposity and are regulated by fasting and feeding

Mutant mice that are unable to produce leptin fail to undergo normal puberty

When these mice are given leptin, all aspects of the reproductive system are stimulated and fertility ensues

51
Q

What is the Melatonin Theory of puberty?

A

Melatonin = hormone secreted from the pineal gland, synchronizes circadian rhythms with light/dark cycles

Melatonin inhibits GnRH release**

Puberty may be initiated by a reduction in melatonin secretion

52
Q

What happens if you remove the pineal gland?

A

Precipitates puberty

53
Q

Precocious Puberty is defined as…

A

Development of secondary sexual characteristics before age 8 in girls or 9 in boys

54
Q

Gonadotropin-dependent precocious puberty is characterized by…

A

Increased gonadotropins (LH, FSH)

CNS tumors

Idiopathic in 90%

55
Q

Gonadotropin-independent precocious puberty is characterized by…

A

Normal gonadotropins, but increased gonadal hormones

Testicular disorders: androgen secreting tumors

Ovarian disorders: estrogen secreting tumors

5x more frequent in girls

56
Q

How do you treat Gonadotropin-dependent precocious puberty?

A

Long-acting GnRH agonists

Results in initial release of FSH/LH, followed by down-regulation and desensitization of receptors —> reduced gonadotropins, reduced sex steroids, and biologic effects

57
Q

How do you treat gonadotropin-independent precocious puberty?

A

Surgical tumor removal

58
Q

Delayed puberty is defined as …

A

Lack of physical maturation 2 SD beyond mean onset

Can be either hypogonadotropic hypogonadism or hypergonadotropic hypogonadism

59
Q

What is hypogonadotropic hypogonadism?

A

Gonadotropin deficiency

Low gonadotropins —> low gonadal hormones

Deficiency of pulsatile release of gonadotropins

Ex: Kallman’s Syndrome

60
Q

What is hypergonadatropic hypogonadism?

A

PRIMARY gonadal failure

Low gonadal hormones result in high gonadotropins due to lack of negative feedback (gonadal streak)

Ex: Turner’s Syndrome or Klinefelter’s Syndrome

61
Q

Failure of fetal migration of GnRH neurons to the hypothalamus

A

Kallman’s Syndrome, delayed puberty due to hypogonadotropic hypogonadism

Lack of pubertal development, associated with short stature and anosmia

62
Q

Condition associated with anosmia due to a genesis or hypoplastic of the olfactory bulbs and tracts

A

Kallman’s Syndrome

63
Q

Treatment for Kallman’s Syndrome?

A

Supplemental sex-steroid (estrogen or testosterone, later GnRH for reproductive capacity)

64
Q

What is Turner’s Syndrome

A

XO hypergonadotropic hypogonadism

Female genital tract forms but no functional gonads

Associated with short stature and delayed or absent puberty and amenorrhea

A type of primary gonadal failure due to absence of negative feedback

65
Q

What is the treatment for Turner’s Syndrome?

A

GH first, then supplemental sex steroids

66
Q

Most common form of primary testicular failure

A

Klinefelter’s syndrome (47, XXY)

Due to absence of negative feedback —> feminization

67
Q

Complications of Klinefelter’s syndrome

A

Germ cell tumors
Breast cancer
Osteoporosis

68
Q

Treatment for Klinefelter’s Syndrome

A

GH first and then supplemental sex steroids

69
Q

Increased gonadotropins (LH, FSH) —> increased gonadal hormones

A

Gonadotropin-dependent precocious puberty

70
Q

Normal gonadotropins (LH, FSH) but increased gonadal hormones

A

Gonadotropin-independent precocious puberty

71
Q

Low gonadotropins (LH, FSH) result in low gonadal hormones

A

Hypogonadotropic hypogonadism

Kallman’s Syndrome

72
Q

Low gonadal hormones result in high gonadotropins due to lack of negative feedback

A

Hypergonadotropic hypogonadism

Turners and Klinefelters

Phys II Unit III (5 decks)

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