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Repro > HPG axis 2 > Flashcards

HPG axis 2 Flashcards

1
Q

what do gonads produce?

A

mature gametes

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2
Q

what do testes produces?

A

spermatozoa

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3
Q

what do ovaries produce?

A

oocytes

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4
Q

what is puberty?

A

the transition from a non-reproductive to a reproductive state

  • breast development in females, increased testicular volume in males.
  • secondary characteristics develop
  • profound physiological changes
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5
Q

do both secondary and primary sexual characteristics develop in puberty?

A

no, primary are present at birth

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6
Q

what are the 2 endocrine events of puberty?

A

adrenarche and gonadarche

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7
Q

what is adrenarche?

A

change in adrenal androgen secretion due to cellular remodelling of adrenal gland

  • secretion of DHEA and DHEAS from the zona retucularis
  • no known trigger
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8
Q

what is pubarche?

A

the result of adrenarche

-appearance of pubic / axillary hair resulting from adrenal androgen secretion

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9
Q

what is pubarche associated with?

A

acne, due to increased sebum production

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10
Q

when does gonadarche occur?

A

Several years after adrenarche (typically ~11 yrs of age)

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11
Q

what is gonadarche?

A
  • Reactivation of hypothalamic GnRH

- Activation of gonadal steroid production production of viable gametes and ability to reproduce

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12
Q

when does GnRH secretion occur in puberty?

A
  • Pulsatile GnRH secretion in foetus until 1-2 years postnatally when ceases
  • GnRH neurones ‘restrained’ during postnatal period, 10 years or more
  • Re-activation at ~11 years
  • At puberty a gradual rise in pulsatile release of GnRH
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13
Q

there is a nocturnal rise in which hormone?

A

GnRH

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14
Q

what happens with anorexia nervosa or intensive physical training?

A
  • Reduced response to GnRH
  • ↓gonadotrophin levels
  • Amenorrhea
  • Restored when nourished / exercise stopped
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15
Q

what is required for menarche (first occurrence of menstruation)?

A

a certain fat body weight

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16
Q

types of KISS1R mutations?

A

inactivating and activating mutations

17
Q

what do inactivating mutations of KISS1R cause?

A
  • Hypogonadism
  • Failure to enter puberty
  • Hypogonadotrophic hypogonadism
18
Q

Hypogonadotrophic hypogonadism

A

No GnRH being released, so no LH or FSH aren’t being released, resulting in a hypogonadotrophic status. No positive drive to testis or ovary to produce follicles or mature sperm.

19
Q

what do activating mutations of KISS1R cause?

A

overactive receptor that acts in the absence of a ligand

-precocious puberty (puberty occurs early)

20
Q

what do ghrelin and leptin regulate?

A

kisspeptin production

21
Q

what is consonance?

A
  • smooth ordered progression of changes

- puberty follows specific order of changes, individual will always follow this pattern regardless of how long it takes

22
Q

physical changes in girls during puberty

A
  • Breasts enlarge
  • Pubic/axillary hair
  • Uterus enlarges, secretions in response to E2
  • Uterine tubes
  • Vagina
  • Cervical changes
  • Height
  • Body shape
  • HPG axis, increase in ovarian size and follicular growth
  • Menarche
  • Fertility
23
Q

physical changes in boys during puberty

A
  • External genitalia, increase in testicular volume, growth of penis, scrotum, scrotal skin changes
  • Vas deferens, lumen increases
  • Seminal vesicles & prostate
  • Facial/body hair
  • Pubic / axillary hair
  • Larynx, androgens enlarge larynx, Adams apple, voice deepens
  • Height
  • Body shape
  • Onset of fertility
24
Q

what is the Adams apple?

A

projection of thyroid cartilage

25
Q

what does testosterone from Leydig cells stimulate in puberty?

A

stimulates meiosis & spermatogenesis in Sertoli cells

26
Q

are boys fertile at the beginning of puberty?

A

yes

27
Q

what is involved in a growth spurt?

A

a complex interaction between growth hormone and oestrogen

-earlier in girls

28
Q

what effect does oestrogen have on epiphyseal growth?

A

a biphasic effect

  • Low levels = linear growth & bone maturation
  • High levels = epiphyseal fusion
29
Q

Psychological changes in puberty?

A
  1. Increasing need for independence
  2. Increasing sexual awareness/interest
  3. Development of sexual personality
30
Q

precocious puberty

A

Development of any secondary sexual characteristic before the age of 8 in girls and 9-10 in boys

31
Q

premature activation of HPG axis

A
  1. Gonadotrophin-dependent precocious puberty – consonance
    - Excess GnRH secretion - idiopathic or secondary
    - Excess gonadotrophin secretion - pituitary tumour
  2. Gonadotrophin-independent precocious puberty - loss of consonance
    - Testotoxicosis - activating mutation of LH receptor
    - Sex steroid secreting tumour or exogenous steroids
32
Q

what is the most common gonadotrophin independent precocious puberty?

A

McCune Albright syndrome

33
Q

what is McCune Albright syndrome?

A

café au lait skin pigmentation

  • g alpha s subunit mutation, activates LH and FSH pathways
  • GNAS1 gene mutations
  • also side effects because of other hormone pathways being activated
34
Q

what is pubertal delay?

A

-absence of secondary sexual maturation by 13yrs in girls or 14yrs in boys
OR
-absence of menarche by 18yrs

35
Q

give 3 reasons for delayed HPG axis activation?

A
  1. Constitutional delay
    affecting both growth and puberty. Approx. 90% of all pubertal delay cases.
    ~10X more common in boys
    secondary to chronic illness e.g., diabetes, cystic fibrosis.
  2. Hypogonadotrophic hypogonadism (low LH and FSH)
    Kallman’s syndrome (X-linked KAL1 gene, impaired GnRH migration),
    Other mutations causing defects in GnRH production
  3. Hypergonadotrophic hypogonadism (high LH and FSH)
    Gonadal dysgenesis and low sex steroid levels:
    gonadal dysgenesis with normal karyotype, viral e.g. mumps
36
Q

kleinfelters syndrome genotype

A

XXY

37
Q

turners syndrome genotype

A

XO

  • ovarian streak (underdeveloped)
  • being shorter than normal

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