Reproduction: Hypothalamic/Pituitary/Gonadal Axis II Flashcards

1
Q

What is puberty?

A

Transition from a non-reproductive to a reproductive state in both males and females

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2
Q

What is the clinical defintion of puberty in both males and females?

A
  • Clincal definition in females is breast development
  • Clinical defintion in males is increased testicular volume
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3
Q

What are the 2 endocrine events that contribute to puberty?

A
  • Adrenarche
  • Gonadarche
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4
Q

What event is induced once as a result of adrenarche?

A

Puberarche

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5
Q

What is Adrenarche?

A

A change in adrenal androgen secretion due to the remodelling of the adrenal gland

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6
Q

What are the main adrenal androgens that see an increase in secretion as a result of adrenarche?

A
  • Dehydro-epiandrosterone (DHEA)
  • Dehydro-epiandrosterone sulphate (DHEAS)
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7
Q

During adrenarche does the level of secretion in another other adrenal androgen change apart from DHEA and DHEAS?

A

No, only secretion of DHEA and DHEAS is changed (increased) durinf adrenarche

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8
Q

What area of the adrenal cortex are DHEA and DHEAS produced and secreted on?

A

Zona reticularis of adrenal cortex

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9
Q

What is puberarche?

A

The appearance of pubic hair/axillary hair due to the increase in adrenal androgen secretion durinf adrenarche

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10
Q

What process is puberarche associated with?

A

Increased sebum production which reults in acne

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11
Q

What other reasons are there for the acne seen during puberarche?

A
  • Infection
  • Abnormal keratinization of the skin
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12
Q

What is Gonadarche?

A
  • The reactivation of the HPG axis at puberty
  • Gradual increase in pulsatile release of GnRH which results in the production of viable gametes
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13
Q

Why does the HPG axis need to be reactivated as a result of Gonadarche?

A
  • HPG axis fist activates at 16th gestational week to ensure correct sexual differentiation
  • Remains active during first 2 postnatal years and then shuts down for about 10 years
  • HPG axis needs to be reactivated via maturation of GnRH neurons to ensure production of mature gametes
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14
Q

Why is LH used to study the behaviour of GnRH within the body rather than GnRH itself?

A
  • LH mimics behaviour of GnRH within the body
  • GnRH only released into hypophyseal portal circulation so incredibly difficult to take GnRH samples directly
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15
Q

Describe the pattern of GnRH release throughout puberty

A
  • Reactivation of HPG axis during early puberty first results in nocturnal rise in GnRH release
  • THis then gradually causes an increase in GnRH pulsatile release throughout the day until you get a consistant pulsatile release of GnRH throughout 24 hours during late puberty
  • Nocturnal rise stil present at late puberty
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16
Q

What are the main ideas for what it is exactly that stimulates the onset of puberty?

A
  • Kisspeptin
  • Body fat/nutrition
17
Q

How are reproductive function and nutrition linked?

A
  • It’s been shown that anorexic individuals and athletes have a reduced response to GnRH
  • This results in a decrease in Gonadotrophin hormone levels (LH and FSH)
  • Amenorrhea in females (absence of menstral cycle)
  • When the diets of the anorexic individuals returned to normal and when athletes stopped exercise their menstrul cycle returned and reproductive function went back to normal
18
Q

What does the body fat hypothesis state?

A
  • States that you need at least 17% body fat to induce menarche (first menstral cycle) and 22% in order to maintain female reproductive ability
19
Q

Explain how both Ghrelin and Leptin may play a role in the onset of puberty?

A
  • Ghrelin secreted from the gut and leptin secreted from adipose tissue are able to regulate secretion of kisspeptin from the hypothalamus
  • Secretion of kisspeptin leads to activation of rest of HPG axis which results in sexual maturation (production of mature gametes from gonads)
20
Q

How are reproductive function and kisspeptin linked?

A
  • Mutations that inactivate kisspeptin receptor or mutations that inactivate kisspeptin gene lead to:
    • Hypogonadism - Small gonadal structures
    • Failure to enter puberty
  • Mutations that activate the kisspeptin receptor without binding of kisspeptin lead to:
    • Precocious puberty (early puberty)
21
Q

Hypogonadism and failure to enter puberty are features of what disorder?

A

Hypogonadatrophic hypogonadism

22
Q

What is consonance?

A

A smooth ordered progression of pubertal chnages that occur during puberty

23
Q

What is the order of pubertal chnages that occur during male puberty?

A
  1. Genital development begins
  2. Growth of pubic hair begins
  3. Peak height spurt
  4. Genitalia fully developed
  5. Pubic hair fully developed
24
Q

What is the order of pubertal changes that occur in females?

A
  1. Breast bud develops
  2. Pubic hair develops
  3. Peak height spurt
  4. Menarche (first menstral cycle)
  5. Pubic hair fully developed
  6. Breasts fully developed
25
Q

What are some of the physical changes that occur in girls during puberty?

A
  • Breast enlargement
  • Growth of pubic/axillary hair
  • Uterus enlarges
  • Cytology changes in uterine tubes, cervix and vagina - cells in these area begin to produce secretions in response to Oestrogens
  • Re-activation of HPG axis
  • Menarche
  • Fertility
26
Q

Why aren’t females classed as fertile once menarche begins?

A
  • Although menarche has occured HPG axis still has to be re-activated in order to induce follicle growth and recruitment
  • This means the first few menstral cycles won’t release an egg cell
27
Q

What are some of the physical changes that occur in males during puberty?

A
  • External genitalia develop - increase in testicular volume
  • Lumen of vas deferens increases
  • Secretions from seminal vesicles and prostate
  • Enlargement of the larynx
  • Onset of fertility - boys are fertile once puberty starts
28
Q

How do oestrogens result in the growth spurt seen during puberty?

A
  • At first low levels of oestrogens result in linear growth and maturation of bones
  • Then high levels of Oestrogens result in bone fusion (marks end of bone growth)
29
Q

What are the 2 types of pilosebaceous units (PSUs)?

A
  • Sebaceous PSUs
  • Vellus PSUs
30
Q

How do androgens affect the different types of pilosebaceous units?

A
  • Androgens cause increased secretion sebum from sebaceous pilosebaceous units which leads to acne
  • Androgens cause the vellus pilosebaceous units to differentiate into terminal pilosebaceous units or the APO-pilosebaceous unit
  • Terminal PSUs cause beard hair growth
  • APO-PSUs lead to pubic/axillary hair growth
31
Q

What psychological changes occur during puberty?

A
  • Increasing need for independence
  • Increasing sexual awareness/interest
  • Development of sexual personality
32
Q

What is precocious puberty?

A
  • Development of any secondary sexual characteristic before the age of 8 in girls and before the age of 9-10 in boys
33
Q

What are the two types precocious puberty?

A
  • Gonadotrophin-dependent
  • Gonadotrophin-independent
34
Q

What are some of the characterististics of gonadotrophin-dependent precocius puberty?

A
  • Excess GnRH secretion
  • Excess gonadotrophin hormone secretion
35
Q

What are some characteristics of gonadotrophin-independent precociuos puberty?

A
  • Occurs when the gonads produce hormones at an usually high rate
  • This results in gonadal maturation occuring too early which results in mature gamete production occuring too early
36
Q

McCune albright syndrome is a cause of gonadotrophin-independent precocius puberty. How does McCune albright syndrome lead to precocious puberty?

A
  • Mutation in the GNAS1 gene causes hyperactivation of all G protein-couplled signalling pathways
  • This results in abnormal amounts of FSH, LH and GnRH to be produced leading to precocoius puberty
37
Q

What is pubertal delay?

A
  • Absence of sexual maturation by the age of 13 in girls and 14 in boys
  • Alos absence of menarche by age 18 in girls
38
Q

What are the different types of pubertal delay?

A
  • Constitutional delay
  • Pubertal delay due to Hypogonadotrophic gonadism
  • Pubertal delay due Hypergonadotrophic gonadism
  • ALL 3 RESULT IN DELAYED HPG-AXIS ACTIVATION
39
Q

How does kallman’s syndrome lead to hypogonadotrophic hypogonadism?

A
  • Kallman’s syndrome caused by mutation in X-linked KAL1 gene
  • Mutation in this gene results in impaired migration of GnRH neurons to the hypothalamus