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Unit 7 > Endocrinology of Puberty and Fertilisation > Flashcards

Endocrinology of Puberty and Fertilisation Flashcards

1
Q

What is the difference between primary and secondary sex characteristics?

A

Primary sex characteristics are present from birth (gonads, internal/external genitilia)
Secondary sex characteristics develop during puberty.

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2
Q

At what stages of life are humans considered fertile and infertile.

A

Infertile as an infant and juvenile
Becomes fertile is adolescence during puberty
Females become infertile at menopause
Men arguably become subfertile in eldery years, infertile until very elderly.

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3
Q

What type of hormones are oestrogen, progesterone and testosterone?

A

Steroid

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4
Q

How does the endocrine system bring about changes in the body?

A

Alters gene expression in cells
Release chemicals for transport in the bloodstream
Release hormones that alter metabolic rate of tissue and organs
Effects can last days, hours or even longer.

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5
Q

What are the principles of endocrine signalling?

A

1) stimulus is detected by endocrine cells
2) A hormone is secreted into the blood stream
3) Hormone travels to effector site with the appropriate receptors (may be distant)
4) Hormone binds to receptors and brings about an effect

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6
Q

What can be a stimulus for an endocrine gland?

A

A change in the internal or external environment.

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7
Q

What are primary endocrine organs?
What are some examples?

A

Organs solely responsible for hormone secretion
Hypothalamus, pituitary, thyroid, pancrease, pineal and parathyroid gland

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8
Q

What are secondary endocrine organs?
What are some examples?

A

Organs that have a wide range of biological processes in addition to secreting hormones to mantain their primary function.
Heart, thymus, GI tract, kidneys and gonads

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9
Q

What are the three different classes of hormones?

A

Peptide
Steroid
Amine

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10
Q

Give an overview of the structure, affinity and mechanism of action of peptide hormones.

A

Consists of peptide chains, sometimes in a quarternary structure
Hydrophilic
Stored in secretory vesicles (produced before stimulation) and released upon simulation, most travel freely in the blood.

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11
Q

What are some examples of peptide hormones?

A

GnRH
LH
FSH
ADH
Prolactin
Oxytocin
hCG

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12
Q

Give an overview of the structure, affinity and mechanism of action os steroid hormones.

A

Steroid hormones are produced by cholesterol
Hydrophobic
Synthesised upon stimulation of biosynthetic enzymes. Diffuse across the plasma membrane
Travel bound to plasma proteins.

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13
Q

What are some examples of steroid hormones?

A

Testosterone, oestrogen, progesterone, aldosterone

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14
Q

Give an overview of the structure, affinity and mechanism of action of amine hormones.

A

Amine hormones are produced from tyrosine
They can be hydrophilic or hydrophobic
Hence may be premade and stored in vesciles, then released on stimulation freely into the blood
Or may be made on stimulation, diffuse across the cell membrane and travel in the blood bound to plasma proteins.

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15
Q

What are some examples of amine hormones?

A

(Nor)adrenaline, dopamine, T3 and T4

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16
Q

How do steroid hormones bring about cellular changes and binding to their receptor?

A

Diffuse to the cell membrane and bind to a cytoplasmic or nuclear receptor.
Receptor hormone complex acts are a transcription factor to alter gene expression

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17
Q

How do protein hormones go about binding to their receptor and causing cellular changes?

A

Bind to cell surface receptors
Activate second messengers which activates a biochemical pathway within the cell, that may release stroed compounds or alter genes expression

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18
Q

How can endocrine cell activity be controlled?

A

By negative/positive feedback loops
By latering the target cells sensitivity to hormone or levels of hormone secreted.

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19
Q

How can target cells change their sensitivity to a hormone?

A

Change in receptor affinity for ligand by covalent modification
Change in the number of receptors.

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20
Q

Why does GnRH need to be secreted in a pulsatile manner to stimulate LH and FSH secretion?

A

Keeps levels of circulating GnRH low then peak in cycles.
Prevents target receptors cells from decreasing sensitivity to GnRH.

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21
Q

What are the primary sex characteristics in females?

A

Gonads - ovaries
Internal genitilia - uterus, fallopian tubes, cervix, upper vagina
External genitilia - labia minora, labia majora, clitoris

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22
Q

What are the primary sex characteristics in males?

A

Gonads - testes
Internal genitilia - epididymis, vas deferens, seminal vesciles
External genitilia - scrotum, glands penic, scrotum

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23
Q

What are gonads?

A

The part of the reproductive system that produces haploid cells by meisosis for use in sexual reproduction

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24
Q

What is the key turning point in foetal development between male and female genitilia?

A

All foetuses originally develop as a female
Eventually, in males, the SRY gene on chromosome Y is expressed, this causes somatic cells of the genital ridge to become testis.
Testis produce testosterone and Mullerine INhibiting Hormones (MIH) triggering male genital development
Without SRY ovaries will develop by default, do not require ovarian endocrine activity.

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25
Q

What pathway in the foetus leads to male primary sexual characteristics?

A

Genome= XY so contains SRY gene
Testis Determining Factor causes the primordial gential ridge to develop in testis
Testosterone (leydig cells) causes the common primorida to become male external genitilia in the presence of Dihydrotestosterone, also causes the Wolffian duct to become male internal genitilia
Mullerian INhibiting Hormone (sertolie cells) causes the mullerian duct to degenerate.

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26
Q

What foetal development pathway leads to the development of the female primary sex characteristics?

A

Genome: XX - so lacks SRY gene
Female gonads develop
Ovarian endocrine activity is not yet required.
The absense of testis endocrine activity allows the mullerine ducts to develop into the internal female genitlia and the wolffian ducts degerenrate.
The common primordia become the female external genitalia.

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27
Q

What are the key hormones involved in the development of male primary sex characteristics?

A

Testosterone
Mullerine Inhibitng Hormone
Dihydrotestosterone

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28
Q

Explain the inheritance pattern of androgen insensitivity syndrome?

A

X linked recessive disorder
Females are carrier, male offspring have a 50% chance of inheriting and expressing AIS from the mother
This is because the gene coding for androgen receptors is located on the x-chromosome.

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29
Q

What causes Androgen Insensitivity Syndrome?

A

Target cells have a decreased sensitivity to androgens such as testosterone due to decreased expression of androgen receptors.
Causes by mutation on X gene for androgen receptors in an XY genome.

30
Q

What are the characteristics of androgen insensitivity syndrome?

A

Male genome but…
Female external genitilia or ambigus genitilia may develop
No internal genitilia as MIH stip produces so stops female genitilia from developing, but not enough testosterone is produced so male internal genitalia does not develop.

31
Q

What is the inheritance pattern of Congenital adrenal Hyperplasia in ….21?

A

Autosomal Recessive
Lacks to gene coding for 21-hydroxylase enzyme

32
Q

What is the mechanism behind 21-OH congenital adrenal hyperplasia in 46 XX?

A

Autosomal recessive mutation leads to decreased or loss of 21-hydroxylase function.
This leads to decreased aldosterone (female sex hormone), decreased cortisol (stress hormone) and increases androgens including testosterone.
Increased androgens causes the male external genitlia to develop alongside the correct female internal genitalia.
The adrenal glands rapdily grow in size, as decreased cortisol activates the negative feedback mechanism, by which more ACTH is produced stimulation adrenal glands to increase secretion of cortisol, but this can not occur instead leading to more androgen secretion.

33
Q

How would a 46 XX patient with 21-OH Congenital Adrenal Hyperplasia present?

A

Internal Female Genitlia - are no sertoli cells so no MIH
External Male Genitilia - due to increases testosterone
High blood pressure and blood salt levels due to reduced aldosterone.

34
Q

What is the biological mechanism behind ‘Guevedoces’ or % alpha reducatse deficiency in a 46 X,Y infant? How will the child present?

A

Develop male internal genitlia as normal as able to produce testosterone and has MIH.
However, lacks 5-ox Reductase so can no convert testosterone to dihydrotestosterone and can not form male external genitalia, instead, the common primordia develops into female external genitalia.
Born with female external genitalia and psuedovagina, at puberty a functional penis and typical penis and male secondary sex characteristics develop.

35
Q

What are some of the effects of having ambiguous external genitalia on the individual?

A
  • Unclear gender assignment at birth as judgement may be inaccurate based on visual external genitalia
    -Ethical debate if external genitalia should be ‘corrected’ in infancy
  • Percieved gender identity from the parents can change the way parents interact with and repons to their child behaviour
  • Confusion around self identity and gender identity.
36
Q

What is the main purpose of puberty?
What are the definitive signs of puberty in males and females?

A

Puberty causes sexual maturation and fertility
Growth of secondary sex characteristics, behavioral changes and growth spurt
Menarche in females and first ejaculation in boys.

37
Q

What is the main hormonal mechanisms behind puberty in males and females?

A

The hypothalamus-pituitary-gonad or HPG axis
The hypothalamus secretes gonadotrophin releasing hormone, this triggers the anterior pituitary gland to pulsatile release the gonadotropins FSH and LH
These travel to the gonads, in biological males results in testosterone production and in biological females results in oestrogen production.
Testosterone and oestrogen inhibts the activity of the anterior pituitary gland and hypothalamus, acting as a negative feedback system.

38
Q

What is the mechanism behind the start of puberty?

A

The hypothalamus activation hypothesis
Before puberty GnRH-producing neurons recieve regulatory inputs that inhibits the hypothalamus from secreting GnRH
Onset of puberty Leptin binds to LepR on Kiss1 neurons in the hypothalamus, these synapse onto GnRH-secreting neurons.
Therefore increases kisspeptin signalling activates more GnRH-secreting hormones leading to more GnRH secretion and eventual increase in sex steroids.

39
Q

Why is the average age of menarche decreasing?

A

Increased nutritional status of women
Increased adipose tissue in younger girls leads to higher levels of leptin which initiates puberty.

40
Q

What cell types do gametes originate from?

A

Primordial germ cells

41
Q

When do oogenesis and spermatogenesis occur?

A

Begins before birth but does not finish until after puberty.

42
Q

What is the role of LH in male puberty?

A

Stimulates Leydig cells to make testosterone, supports spermatogenesis, development of secondary sex characteristics, supports secretory activity of sex glands.

43
Q

What is the role of FSH in male puberty?

A

Stimulates sertoli cells to produce estradiol, androgen-binding protein, inhibin and growth factors needed for spermatogenesis.

44
Q

When does the mitotic division of the primary spermatogonia start for sperm production in males?

A

At puberty

45
Q

What are the different stages of sexual maturation in puberty?

A

Early sexual maturation - low sex steroids
Later sexual maturation - high sex steroids

46
Q

What causes a growth spurt during puberty?

A

Growth Hormone releasing hormone is produces by the hypothalamus
Causes growth hormone release from the pituitary gland.
Growth factors result in increased longitudinal bone growth - growth spurt
Insulin Like Growth Factor 1 - causes fusion the epiphyseal growth plate, results in sessation of longitudinal bone growth

47
Q

What causes the adrenal cortex to release sex hormones?

A

Secretion of ACTH adrenocorticotropic hormone from the pituitary gland.

48
Q

What are the secondary sex characteristics in females?

A

Development of breast tissue
Enlargement of genitalia
Increase in body fat

49
Q

What are the secondary sex characteristics in males?

A

Enlargement of genitalia
Deeo voice
Increase in lean body mass
Increase in strength
Facial hair.

50
Q

What are the effects of testosterone on behavior?

A

Increase in sexual behavior
May increase physical aggression and anger
Maintain mood
Improved cognitive ability
Causes behaviour to improve social status

51
Q

What are the effects of the menstrual cycle on behaviour?

A

increase libido around ovulation
May increase sexual attractiveness to males
Can improve mood
Improves cognitive function.

52
Q

What physiological events must the mesntraul cycle prepare the female reproductive system for?

A

Transport of spermatozoa and fertilisation during the oestrogen dominant part of the cycle (follicular phase).
Supporting implanatation and develop of embryo during progesterone dominaant cycle, called the luteal phase.

53
Q

What is meant by the follicular and luteal phase of a menstraul cycle?

A

Follicular is the first 14 days (of a 28 day cycle) from menses to ovulation
The luteal phase is the last 14 days from after ovulation until the start of menstration

54
Q

What happens in the preantral phase of follicular development?

A

Oocyte has not yet undergone any mitotic division
Granuluse cells prliferation, causing oocyte to gorw in size
Zona pellucida secreted from oocye
Thecal cells develop, increasing oestrogen secretion from granulosa cells
Blood cell develops.

55
Q

What happens in the antral phase of follicular development?

A

This is gonadotrophin dependent stage
Granulosa cells secrete follicular fluid to iform the antral cavity. Follicle increase in size
Secretory activity increases
Morphological changes in follicle

56
Q

What happens in the pre-ovulatory phase of follicular development?

A

Is dependent on LH and Progesterone
First mitotic division in complete
Antral fluid rapidly increases in volume
Hormone-stimulate protease activity.
Develop cortical granules.

57
Q

Give an overview of granulosa cells.

A

Develop from mesnechymal cells
Surround the oocyte and provide nutritional support
Converts androgens made by theca cells in oestrogen in the presence of FSH

58
Q

Give an overview of theca cells

A

Arise from ovarian stroma to surround primary follicles
Prodcues androgens from cholsesterol when stimulated by LH.

59
Q

Describe the hormonal processes of the ovarian cycle follicular phase?

A

Activation the Hypothalamus Pituitary Ovarian Axis
LH and FSH secretion from the pituitary gland triggers the development and growth of many follicles in the ovary.
FSH also triggers oestrogen production in granulosa cells from the thecal androgen precursor
Oestrogens increase expression of FSH receptors on granulosa cells causing the granulosa cells to be more sensitive to oestrogen and proliferate.
Rise in oestrogen and inhibin from granulosa, acts in a negative feedback loop to reduce FSh and LH plateaus.
Only the most advanced follicle can continue to develop in low FSH due to higher FSH receptors.
Oestrogen surges stimulating expression of LH receptors and further proliferation.
At high high concentrations oestrogen changes to a positive feedback mechanism causing LH and FSH surge resulting in ovulation.

60
Q

What is atresia in the ovarian cycle?

A

When FSH levels drop only the dominanat follicles continues to mature.
The less mature follicles lose trophic support and can not develop further - this is atresia

61
Q

What happens to the support cells of the oocyte that are left in the ovary after ovulation?

A

The granulosa and theca cells left in the follicle collapse around a fibrin core to form a corpus luteum

62
Q

What are the hormonal changes int he luteal phase of the ovarian cycle?

A

Ovulation has just occured
LH stimulates progesterone production and oestrogen production decreases.
In the corpus luteum, LH causes increased levels of progesterone and oestrogen.
High level progesteron inhibits LH and FSH preventing further ovulation.
LH decreases, the corpus luteum degrades causing a decrease in progesterone and oestorgen, removing their inhibitory effect
The next cycle can start when gonadotropin release in stimulated again by the hypothalamus

63
Q

What is primary hypogonadism?

A

Also known as hypergonadotrophic hypogonadism
The pituitary gland is able to produces LH and FSH (gonadotrophic hormones) but the gonads do not respond to these signals so decreased testosterone in males, and decreased oestrogen in females.
This means there is no inhibitory effect on the pituitary gland so LH and FSH levels increase rapidly.

64
Q

What are the symptoms of primary hypogonadism in males?

A

Failure to develop male secondary sex characteristics or very late onset puberty
Often have a female type pubic hair pattern, breast development and wider hips.
Long arms and legs.

65
Q

Give some examples of primary hypogonadism

A

Klinefelter’s syndrome - male XXY
Androgen Insensitivity Syndrome - male and female
Turner Syndrome - females with only one X chromosome

66
Q

What is Klinefelter’s syndrome?

A

A sponstaneous chromosome abnormality that effects males.
Genome: 47 XXY
Have decreased levels of testosterone, struggle to develop secondary sex charactetristics, fertility problems, cognitive delays, struggle in social situations, extra breast tissue, taller than expected.
Genital atrophy

67
Q

What are some potential causes of primary hypogonadism?

A

Leydig cell agenesis
Chromosome abnormality
Gene mutation
Latrogenic - illness from medical treatment e.g chemo
Gonad disease/destruction
Cirrhosis - chronic inflammation of liver

68
Q

What is the recommended treatment for primary and secondary hypogonadism?

A

Replacement therapy, often sex steroids (or gonadotrophic hormones in secondary)

69
Q

What is secondary hypogonadism?

A

Also called hypogonadotrophic hypogonadism
Reduced production of LH and FSH from the pituitary glands causes a reduction in sex hormones, such as testosterone
Such as kallmann’s syndrome and hyperprolactinaemia

70
Q

What are some of the potential causes of secondary hypogonadism?

A

Hypothalamus or pituitary gland failure
Genetic
Auto-immune
Latrogenic - caused by medicine such as chemo
Idiopathic - spontaneous with an unknown cause.

71
Q

What is Kallmann’s syndrome?

A

A type of secondary hypogonadism, combined with an impaired sense of smell.
Rare genetic conditions - associated with 25 different genes, more common in males
Results in absent or delayed puberty
Small penis and undescended testes at puberty
Infertility
Reduced growth spurt.

72
Q

How does priamry and secondary hypogonadism present in patients?

A

Absent/delayed puberty
Low libido
Infertility
Gynaecomastia (breast growth in males)
Loss of secondary hair
Genital atrophy.

Unit 7 (20 decks)

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