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Physiology 2 : Reproduction and bones > HPG - axis > Flashcards

HPG - axis Flashcards

1
Q

What do we need to reproduce?

A
  • Correct process of sex determination (genotypic sex) and differentiation (phenotypic sex)
  • Sexual maturation- Puberty
  • Production and storage of sufficient supply of eggs & sperm
  • Correct number of chromosomes in egg and sperm
  • Actual sexual intercourse! Egg & sperm have to be transported and meet
  • Fertilisation, implantation, embryonic and placental development
  • Once delivered, to nurture individual until capable of “independent” life
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2
Q

How is HPG axis the master controller of reproduction?

A 
Gonadal function is controlled via feedback  by:
Hypothalamic & pituitary peptide hormones.
Gonadal steroid (and peptide) hormones.
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3
Q

Hypothalamus (RH)

A

Gonadotrophin Releasing Hormone (GnRH), (kisspeptin)

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4
Q

Pituitary (SH)

A

Follicle Stimulating Hormone (FSH) and Luteinising Hormone (LH)

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5
Q

Gonad

A

(F) Oestradiol (E2), Progesterone (P4), (M) Testosterone, (Inhibin and activin).

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6
Q

Kisspeptine (KISS1/kiss1)

A
  • Role in reproduction recently discovered – 2001 - gatekeeper of puberty
  • Hypothalamic expression- ARC and AVPV
  • Upstream of GnRH
  • Kisspeptin neurons send projections to GnRH neurons, and binding to GPR54 expressed on GnRH neurons
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7
Q

Hypothalamus GnRH

A
  • Synthesised and secreted from GnRH neurons
  • Secreted in a pulsatile fashion-pulse generator orchestrated
  • Hypothalamic expression- ARC and MPN (Parvocellular system)
  • Binds to the GnRH receptor (GnRHR) on gonadotroph cells of the anterior pituitary to stimulate the synthesis and secretion of gonadotrophin hormones- LH and FSH.
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8
Q

Pulsatility

A
  • GnRH is secreted in pulses from hypothalamus every 30-120min.
  • A GnRH pulse stimulates a pulse of LH and FSH secretion from the pituitary.
  • Pulsatile GnRH secretion is vital for stimulation of LH/FSH secretion.
  • Slow frequency pulse favours FSH release, rapid pulse frequency favours LH.
  • Continuous release results in cessation of response.
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9
Q

Therapeutic application of GnRH

A

• Synthetic GnRH – same structure as endogenous GnRH
- pulsatile administration Stimulatory
• GnRH analogues – modified GnRH peptide structure
- Single bolus, long half life, loss of pulsatility  Inhibitory
- Agonists or antagonists

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10
Q

Pituitary to Gonads

A

Ultimate coordination of gonadal function to facilitate viable gamete production (male), growth and development

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11
Q

Gonadotrophin hormones: LH, FSH (hCG)

A

Heterodimeric peptides – common α-subunit and hormone-specific β-subunit
• N-linked carbohydrate side chains required for biological function
• Free subunits have no biological action
• α-subunits are synthesized in excess with β-subunit limiting the hormone concentration
Pulsatile secretion due to pulsatile GnRH release from hypothalamus but pulsatile secretion not necessary for biological activity

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12
Q

Luteinising hormone

A

• Testis:
- stimulation of Leydig cell androgen synthesis
• Ovary:
- theca cell androgen synthesis
- ovulation
- progesterone production of corpus luteum

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13
Q

Follicle-stimulating hormone

A 
• Testis:
	- regulation of Sertoli cell metabolism
• Ovary: 
	- follicular maturation
	- granulosa cell estrogen synthesis
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14
Q

Oestrogens

A
  • Oestradiol and also oestrone
  • Folliculogenesis
  • Positive feedback triggers ovulation
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15
Q

Androgens

A
  • Androstenedione, testosterone, dihydrotestosterone

- Spermatogenesis

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16
Q

Progesterone

A
  • Prepares the uterus for implantation

- Maintains conditions required for the early stages of pregnancy

17
Q

Puberty

A
  • Transition from non-reproductive to reproductive state
  • Breast development in females, and increased testicular volume in males.
  • Secondary characteristics develop (primary are present at birth)
  • Profound physiological changes
  • Profound psychological changes
18
Q

Adrenarche

A

• Change in adrenal androgen secretion due to cellular remodelling of adrenal gland.
- Dehydro-epiandrosterone (DHEA)
- Dehydro-epiandrosterone sulphate (DHEAS)
No change in other adrenal steroids
- Secreted from zona reticularis of adrenal cortex
- No known mechanism for trigger of adrenarche

19
Q

Pubarche

A

Appearance of pubic / axillary hair resulting from adrenal androgen secretion
Associated with:
 sebum production = acne
Infection, abnormal keratinization = acne
If before 8 years (girls) or 9 years (boys)
= PRECOCIOUS

20
Q

Gonadarche

A
  • Several years after adrenarche (typically ~11 yrs of age)
  • Reactivation of hypothalamic GnRH
  • Activation of gonadal steroid production  production of viable gametes and ability to reproduce
21
Q

Gonadarche:GnRH

A

GnRH is synthesised & secreted by specialist hypothalamic centres – GnRH neurones.
HPG axis is first activated at 16th gestational week
• Pulsatile GnRH secretion in foetus until 1-2 years postnatally when ceases
• Re-activation at ~11 years
GnRH neurones ‘restrained’ during postnatal period  10 years or more
At puberty a gradual rise in pulsatile release of GnRH

22
Q

Onset of puberty theories

A

Clear that it is maturational event within the CNS
• Inherent (genetic) maturation of 800-1000 GnRH synthesising neurones?
• Environmental/genetic factors?
• Body fat/nutrition?
• Kisspeptin?

23
Q

Nutrition & body fat

A

• Link between fat metabolism & reproduction
• Anorexia nervosa / intensive physical training
Reduced response to GnRH
↓gonadotrophin levels
Amenorrhea
Restored when nourished / exercise stopped
• Frisch et al.: body fat hypothesis
Certain % fat:body weight necessary for menarche (17%) & required (22%) to maintain female reproductive ability

24
Q

Kisspeptin and puberty

A
  • Inactivating mutations of KISS1R or the gene coding for kisspeptin
  • Hypogonadism
  • Failure to enter puberty
  • Hypogonadotrophic hypogonadism
  • Activating mutations of KISS1R
  • Precocious puberty
25
Q

Tanner stages of puberty

A
  1. Pubic and axillary hair growth (♀♂)
  2. Testicular volume and penile length (♂)
  3. Breast development (♀)
26
Q

Physical changes in girls during puberty part 1

A

Breasts enlarge
thelarche – first outward sign of E2 activity
Pubic/axillary hair
Uterus enlarges, cytology changes, secretions in response to E2
Uterine tubes
Cervical changes

27
Q

Physical changes in girls during puberty part 2

A

• Height
- earlier onset than boys
- peak height velocity (PHV) = 9 cm/y, reached at 12 yrs
• Body shape
• HPG axis
- increase in ovarian size and follicular growth
• Menarche
- not equated with onset of fertility
• Fertility
- in 1st year ~80% menstrual cycles anovulatory, irregular cycles

28
Q

Physical changes in boys during puberty 1

A 
•	External genitalia 
-	increase in testicular volume >4 ml
•	growth of penis, scrotum, scrotal skin changes
•	Vas deferens 
•	lumen increases
•	Seminal vesicles & prostate
•	Facial/body hair 
•	Pubic / axillary hair
29
Q

Physical changes in boys during puberty 2

A 
•	Larynx – 
androgens  enlarge larynx, Adams apple (projection of thyroid cartilage), voice deepens
•	Height 
PHV =10.3 cm/y reached at 14 yrs
•	Body shape
•	Onset of fertility 
testosterone from Leydig cells stimulates meiosis & spermatogenesis in Sertoli cells  
Boys fertile at the beginning of puberty
30
Q

Psychological changes of puberty

A
  1. Increasing need for independence
  2. Increasing sexual awareness/interest
  3. Development of sexual personality
    Later maturation = better adjustment
31
Q

Biphasic effect of oestrogen on ephiphyseal growth

A

Low levels = linear growth & bone maturation

High levels = epiphyseal fusion

32
Q

Growth interaction

A

Complex interaction
Growth hormone
Oestrogen (boys and girls)
Earlier in girls – approx. 2 years

33
Q

Precocious sexual development

A

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

34
Q

Gonadotrophin-dependent (or central) precocious puberty

A

consonance
Excess GnRH secretion - idiopathic or secondary
Excess gonadotrophin secretion - pituitary tumour

35
Q

Gonadotrophin-independent precocious puberty

A

loss of consonance
Testotoxicosis - activating mutation of LH receptor
Sex steroid secreting tumour or exogenous steroids

36
Q

Constitutional delay

A

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

37
Q

Hypogonadotrophic

A

(low LH and FSH)
Kallman’s syndrome (X-linked KAL1 gene, impaired GnRH migration),
Other mutations causing defects in GnRH production

38
Q

Hypergonadotrophic hypogonadism

A

(high LH and FSH)
Gonadal dysgenesis and low sex steroid levels:
gonadal dysgenesis with normal karyotype, viral e.g. mumps

Physiology 2 : Reproduction and bones (13 decks)

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