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Life Cycle > Disorders of Puberty > Flashcards

Disorders of Puberty Flashcards

1
Q

Describe the hypothalamic axis for sex hormones.

A
  1. Hypothalamus secretes GnRH in a pulsatile manner
  2. This stimulates the anterior pituitary to release LH, FSH
  3. This stimulates the gonads (ovaries/testes) to secrete progestrone/estrogen/testosterone
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2
Q

Describe the activity levels of the hypothalamic sex hormone axis over time

A
  • HPG axis is active in fetal development and infancy (mini-puberty)
  • HPG axis then becomes dormant during “juvenile pause” due to inhibitory neurotransmitters acting on hypothalamus
  • HPG re-activates during puberty
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3
Q

What stimulates the hypothamus to re-awaken after juvenile phase?

A

KISS-1 neuron

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4
Q

Compare the levels of FSH and LF before and during puberty

A

Prepuberty: FSH > LH

Puberty: LH > FSH

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5
Q

Describe two laboratory evaluations of puberty

A
  1. Serum sample of LH, FSH
    • High levels confirm puberty, low levels cannot rule puberty out (may have missed a pulse)
  2. If LH/FSH was low, give GnRH analog and measure LH/FSH response
    • If child is not in puberty yet, GnRH will not have an effect (no change in LH, FSH)
    • If child is in puberty, FSH and LH will rise
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6
Q

Estrogen stimulates… (4)

A
  • Breast development
  • Growth/maturation of uterus, vagina, and labia
  • Female fat distribution
  • Menses
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7
Q

Testosterone stimulates…(4)

A
  • Penile and prostate growth
  • Pubic hair
  • Muscle mass
  • Voice change

*This all follows enlargement of testes (mediated by FSH, LH)

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8
Q

What causes bone age advancement?

A

Estrogen!

This is the case for both boys and girls

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9
Q

Define adrenarche.

What does this cause? (3)

A

Adrenarche = when adrenal glands start producing androgens (DHEA, androstenedione)

This causes pubarche (pubic/axillary hair, body odor, and acne)

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10
Q

What is the diagnostic criteria for delayed puberty?

A
  • Onset of puberty after
    • 13 years in girls
    • 14 years in boys
  • OR lack of progression (no menarche/genital growth a few years after starting puberty)
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11
Q

What will best indicate the expected onset of puberty?

A

Bone age

This best represents the body’s physiologic age

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12
Q

What is Hypogonadotropic Hypogonadism?

A

Lack of puberty due to decreased GnRH or LH/FSH

(central)

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13
Q

Describe the growth course in Constitutional Growth Delay (3)

A
  • Growth decelerates in first 2 years, which puts child on a low percentile growth curve
  • Normal linear growth at this lower percentile
  • Onset of puberty is late, but corresponds with bone age (bone age is delayed)
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14
Q

Name 2 genetic causes of Hypogonadotropic Hypogonadism

A

Prader Willi

Kallman Syndrome

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15
Q

What is the pathogenesis of Kallman Syndrome?

What are the two primary symptoms?

A
  • Defective migration of GnRH-releasing neurons and the olfactory bulb, causing low GnRH synthesis in the hypothalamus
  • Sx: anosmia, hypogonadotropic hypogonadism (infertility, failure to complete puberty)
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16
Q

What would GnRH, LH, FSH, estrogen, and testosterone level by in hypergonadotropic hypogonadism?

A
  • Elevated GnRH, LH, FSH
  • Low estrogen/testosterone

*This is primary gonadal failure

17
Q

What is the underlying abnormality in Klinefelter’s?

Name 4 signs/symptoms

A
  • 47, XXY
  • Learning disabilities
  • Eunuchoid body shape (tall, long extremities, gynecomastia, female hair distribution)
  • Testicular atrophy
  • Infertility
18
Q

What is the treatment of hypogonadism?

A

Hormone replacement (testosterone or estrogen+progesterone)

19
Q

What would GnRH, LH, FSH, and testosterone levels be in Kallman syndrome?

A

They would all be low b/c the problem is in the hypothalamus.

20
Q

Describe the defect in placental aromatase deficiency.

What are two symptoms?

A
  • Inability to synthesize estrogens from androgens (due to aromatase defect), leading to high levels of androgens
  • Sx: Masculinization of female (46,XX) infants or maternal virilization
21
Q

Describe the hormones produced due to LH and FSH stimulation

A
  • LH stimulates Leydig cells
    • Leydig cells make testosterone
  • FSH stimulates Sertoli cells
    • Sertoli cells make androgen binding protein, aromatase, inhibin, anti-mullerian hormone (SAANA)
22
Q

Describe the labs seen in Klinefelters related to Leydig and Sertoli dysgenesis.

A
  • Dysgenesis of seminiferous tubules -> abnormal Sertoli cells -> low inhibin levels -> high FSH
  • Abnormal Leydig cells -> low testosterone -> high LH -> high estrogen

Life Cycle (27 decks)

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