Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Life Cycle > HPG Axis and Puberty > Flashcards

HPG Axis and Puberty Flashcards

1
Q

What are the 3 levels of the HPG axis in puberty?

A

H: hypothalamus releases GnRH from neurosecretory neurons stimulated by kisspeptin

P: pituitary releases FSH/LH (gonadotrophin)

G: gonads synthesise and release ESTRADIOL (E2) and PROGESTERONE (P4) (E2 +P4 are predominant in females) and TESTOSTERONE (predominant in males)

N.B. that all 3 sex hormones are produced by both sexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is kisspeptin?

A

peptide hormone
10-54aa in size

kisspeptin neurons send projections to GnRH neurones

GnRN neurons contain kisspeptidn receptors - binding causes release of GnRH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is GnRH and where it is released?

A

small, 10aa peptide hormone
released by neurons into the median eminence

travels to anterior pituitary via the HYPOPHYSEAL PORTAL VESSEL

binds to GnRH-receptors on gonadotroph cells

These then produce LH/FSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Where is the superior hypophyseal artery?

A

connection between the hypothalamus and pituitary

type of portal vessel

delivers blood into capillary network of upper infundibulum

allows access to the anterior pituitary for subsequent activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What fo the role of the hypophyseal veins?

A

carry blood containing pituitary hormones

carried to cardiovascular system for systemic delivery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What blood vessel delivers blood to the posterior pituitary?

A

inferior hypophyseal artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the nature of GnRH secretion? Why is this important?

A

GnRH has PULSATILE secretion
every 30-120mins

GnRH receptor is a GPCR

continuous secretion switches off the HPG axis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What types of GnRH stimulates LH/FSH secretion?

A

SLOW GnRH: FSH release

FAST GnRH: LH release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the generalised structure of gonadotrophins?

A

heterodimeric peptides

common alpha subunit (92aa) and hormone-specific beta subunit

beta subunits are less abundant and therefore regulate the specific [hormone]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the structure of LH?

A

common alpha subunit (92aa)

LH beta subunit (121aa)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the structure of FSH?

A

common alpha subunit (92aa)

FSH beta subunit (110aa)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the structure of hCG?

A

common alpha subunit (92aa)

hCG beta subunit (145aa)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What post-translational modifications allow full biological potency of the gonadotrophin?

A

LH/FSH: N-linked glycosylation

hGH: O-linked glycosylation

=> function may vary through pregnancy/menstrual cycle

note that free subunit monomers carry no biological function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the 2 main endocrine events in puberty?

A
  • Adrenarche + Pubarche
  • Gonadarche
    (together make up puberty, but are independently regulated)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is adrenarche?

A

change in adrenal secretion
caused by adrenal gland remodelling from childhood

ZONA RETICULARIS: develops as independent zone as adrenarche occurs

secretion of DHEA (sulfated and non-sulfated) lead to pubarche
[at 10-20yo]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the proposed triggers for adrenarche?

A

largely unknown
leptin or insulin signalling
may be related to body mass
physiological remodelling of adrenal glands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the main stages of puberty?

A
  1. ADRENARCHE maturation of cells in adrenal gland
  2. release of androgens
  3. This causes PUBARCHE - appearance of pubic and axillary hair

[GONARCHE follows on from pubarche, driven by HPG axis]

  1. synthesis and secretion of LH/FSH
  2. Activation of gonadal function
  3. LH: gonadal steroidal synthesis and secondary sex characteristics
  4. FSH: testis growth (male) and folliculogenesis with steroid synthesis (female)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the function of DHEAS in adrenarche?

A

= sulfated dehydroepiandrosterone

transported to gonads/adrenals where it is converted to testosterone or DHT
occurs in Leydig cells in M

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is pubarche?

A

appearance of pubic or axillary hair (from androgen secretion during adrenarche)

Acne: increased sebum production
infection can be caused by abnormal keratinisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

When is pubarche considered to be ‘precocious?’

A

GIRLS: <8 yo

BOYS: <9yo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are pilosebacious units?

A

= PSUs
= hair + hair follicle + error pills muscles + sebaceous glands

deposit sebum on hairs
bring hair to surface along the hair shaft

22
Q

What does a sebaceous PSU consist of?

A

large sebaceous gland

secrete sebum under androgen influences

acne develops when pores are blocked or become infected

23
Q

What structures go on to become moustache and beard hair?

A

terminal PSUs

24
Q

What are villus pilosebaceous units?

A

can differentiate into 2 types of hair: terminal PSU or apocrine PSU
occurs under androgen exposure

25
What is an ECCRINE GLAND?
type of simple sweat gland produces most sweat not associated with hair follicles
26
What are APOCRINE GLANDS?
present in the skin scent glands secretions usually have an odour located in the armpits and groin go on to form pubic and axillary hair
27
What is GONADARCHE?
HPG axis first activates during 16th gestational week pulsatile GnRH in foetus occurs until 1-2 years (postnatally) GnRH neurons restrained between 2-10yo only reactivated during gonadarche (due to pulsatile GnRH release) increased kisspeptin promotes GnRH release ultimately stimulates gonadal steroidogenesis this will lead to viable gamete production
28
What is the best method of monitoring GnRH secretion?
Can measure serum LH levels (more accurate than FSH levels)
29
How does GnRH release change through puberty?
becomes a more consistent pulsatile release in the adult, pulse frequency occurs during the day
30
What are the epiphyses? What is fusion?
rounded ends of bones (=growth plate) initially form separately to the long bones, will eventually fuse with main shaft of long bone initially low oestrogen levels promote bone growth (linear) and mediate rapid growth spurt then, fusion occurs when the oestrogen levels rapidly increase during puberty
31
What mediates the pubertal growth spurt?
complex interaction between GH and Oestrogen occurs ~2yrs earlier in F than M
32
What is the relationship between oestrogen and epiphyseal growth?
low [oestrogen] = when HPG reawakens, promotes linear growth INITIAL GROWTH SPURT high [oestrogen] = epiphyseal FUSION at growth plates GROWTH STOPS
33
What stimulates pubertal onset?
[not entirely known] maturational event within CNS - GENETIC: maturation of GnRH synthesising neurons, also epigenetic regulation - NUTRITION: earlier puberty as neutron improves. Malnutrition delays puberty, 17-18% body fat needed to initiate puberty and 22% to maintain menstrual cycle (link to leptin levels?) - KISSPEPTIN: variants in kisspeptin may alter puberty initiation (GoF vs LoF)
34
What is consonance?
= smooth ordered progression of changes in puberty this will remain regardless of how long each pubertal transition takes
35
What are the physical changes that occur in BOYS during puberty?
External genitalia - increase in testicular volume >4ml growth of penis, scrotum, scrotal skin changes Vas deferens - lumen increases. Seminal vesicles & prostate - maturation preparation for secretion. Facial / body hair Pubic / axillary hair Larynx - androgens enlarge larynx. Adams apple (projection of thyroid cartilage), voice deepens Height - PHV = 10.3 cm/year reached at 14 years Body shape - broadening of shoulders and chest; shoulders wider than hip. Onset of fertility - testosterone from Leydig cells stimulates meiosis & spermatogenesis in Sertoli cells boys fertile at the beginning of puberty.
36
What are the physical changes that occur in GIRLS during puberty?
Breasts enlarge - thelarche – first outward sign of estrogen activity represents reawakening of HPG axis. Pubic/axillary hair Uterus enlarges - myometrium responds to estrogen. Endometrium, uterine tubes, cervix - differentiation & maturation. Height - earlier onset than boys peak height velocity (PHV) around 9 cm/year, reached at 12 years. Body shape - widening of the hips. Ovary - increase in ovarian size and follicular growth. Menarche - not equated with onset of fertility but late into puberty at Tanner stage IV. Fertility - in 1st year ~ 80% menstrual cycles anovulatory, irregular cycles.
37
What are the Tanner stages?
= pubertal development stages 1 -5 stage 1: pre-pubescent, puberty starts at stage 2 stage 5: end of puberty (in F, this is marked by onset of menses)
38
What psychological changes occur in puberty?
- increasing need for independence - increased sexual awareness/desire - development of sexual personality
39
What is 'central precocious puberty?'
= Gonadotropin-DEPENDENT precocious puberty CONSONANCE MAINTAINED - excess GnRH secretion: idiopathic or secondary - excess gonadotrophin secretion: pituitary tumour accelerated linear growth (for age), advanced bone growth, increased LH/FSH/E2 and testosterone
40
What is the Rx for central precocious puberty?
- case-by-case assessment - dependent on age, psychological benefits, parent wishes, and expectations GnRH analogues: suppress puberty until 11-12yo (if appropriate) Surgery, radiotherapy or chemo also available
41
What is the consequence of a hypothalamic hamartoma?
found in 33% of patients with central precocious puberty unclear aetiology, but proposed to be non-physiological GnRH secretion HAMARTOMA = focal malformation, usually benign. resembles a neoplasm in the tissue of its origin
42
What is 'peripheral precocious (pseudo) puberty'?
Gonadotrophin-INDEPENDENT peripheral precocious puberty Hallmark: secondary characteristics develop BEFORE gonadal development Associated with: - suppressed LH/FSH - elevated oestrogen and testosterone
43
What are the different types of peripheral precocious puberty?
TESTOXICOSIS: activating mutation in LH receptor causes early androgen synthesis 9=(in Leydig/Theca cells) No FSH increase so no spermatogenesis Sex steroid secreting tumour/exogenous steroids: secondary sexual characteristics McCUNE ALBRIGHT SYNDROME: constitutive activation of adenylate cyclase. Causes hyperactivity of signalling pathways including those of gonadotrophin hormones CONGENITAL ADRENAL HYPERPLASIA (CAH): compensatory androgen overproduction (deficient in cortisol)
44
What is McCUNE-ALBRIGHT SYNDROME?
rare genetic disorder affects skins colour (cafe au lait), bones and hormone imbalance caused by activating mutations in alpha subunit of G(as) subunit of GPCR LH and hCG receptors: GPCR causes autonomous endocrine function and fibrous dysplasia
45
What is pubertal delay?
= absence of secondary characteristics by 14yo (M) and 13yo (F) or absence of menarche by 18o (F)
46
What are the different types of pubertal delay?
- constitutional delay - HYPOgonadotrophic hypogonadism (low LH/FSH) - HYPERgonadotrophic hypogonadism (high LH/FSH)
47
What is constitutional pubertal delay?
``` affects both growth and puberty 90% of all pubertal delay cases M > F (x10 in M) polygenic can occur secondary to chronic illness e.g. DM, CF ```
48
What is HYPOgonadotrophic hypogonadism?
= low LH/FSH KALLMANN'S SYNDROME (X-linked KAL gene: impairment of GnRH neurone migration) Hypopituitarism, impaired gonadotrophins high dose or long term expo to opioid or steroid medicines other genetic disorders
49
What is HYPERgonadotrophic hypogonadism?
= high LH/FSH insensitivity to LH/FSH from gonadal dysgenesis Low sex steroid levels (low negative feedback and high gonadotrophins) Congenital: - KLINEFELTER'S SYNDROME (XXY sex chr) 1:500 males - TURNER'S SYNDROME (X- sex chr) 1:3000 females Gonadal dysgenesis with normal karyotype e.g. mumps
50
What are the (positive) acute phase proteins?
=>INCREASE during inflammation - CRP - procalcitonin - ferritin - alpha-1 antitrypsin - caeruloplasmin - serum amyloid A - serum amyloid P component - haptoglobin - complement
51
What are the (negative) acute phase proteins?
=> DECREASE during inflammation - albumin - transthyretin (aka prealbumin) - transferrin - retinol binding protein - cortisol binding protein

Life Cycle (29 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions