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Endocrinology > Puberty > Flashcards

Puberty Flashcards

1
Q

Human life cycle of fertility?

A
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2
Q

Basic principles of endocrine signalling?

A
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3
Q

Primary endocrine organs (where endocrine signals released)?

A

-Hypothalamus
-Pituitary
-Thyroid
-Adrenal
-Pancreas
-Pineal gland
-Parathyroid

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4
Q

Secondary endocrine organs (where endocrine signals released)?

A

-Heart
-Thymus
-GI tract
-Kidneys
-Gonads

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5
Q

What are the 3 classes of hormones?

A

*Protein/peptide
*Steroid
*Amine

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6
Q

Examples of protein/peptide hormones?

A

-GnRH
-LH
-FSH
-ADH
-Prolactin
-Oxytocin
-hCG

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7
Q

Affinity of protein/peptide hormones?

A

= Hydrophilic (= high water solubility)
–> so travels freely in blood without need for carrier protein

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8
Q

Synthesis of protein/peptide hormones?

A

Stored in secretory vesicles - released upon stimulation

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9
Q

Mode of transport of protein/peptide hormones?

A

Freely in blood - due to hydrophilic nature (except GH, IGF1 & IGF2)

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10
Q

Structure of steroid hormones?

A

Produced from cholesterol

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11
Q

Examples of steroid hormones?

A

-Testosterone
-Oestrogen
-Progesterone
-Aldosterone

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12
Q

Affinity of steroid hormones?

A

= Hydrophobic (= low water solubility) - so need carrier protein to carry between different tissues

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13
Q

Synthesis of steroid hormones?

A

-Synthesised upon stimulation of biosynthetic enzymes
-Diffuse across plasma membrane – no storage!

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14
Q

Mode of transport of steroid hormones?

A

Bound to plasma proteins - due to hydrophobic nature

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15
Q

Structure of amine hormones?

A

Produced from tyrosine (AA)

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16
Q

Examples of amine hormones?

A

-Nor)adrenaline
-Dopamine
-T3
-T4

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17
Q

Affinity of amine hormones?

A

Either - hydrophilic or hydrophobic

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18
Q

Synthesis of amine hormones?

A

Either - synthesis upon stimulation or stored in secretory vesicles

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19
Q

Mode of transport of amine hormones?

A

Either - travel freely in blood (if hydrophilic) or bound to plasma proteins (if hydrophobic)

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20
Q

Summary of:
-Structure
-Examples
-Affinity
-Synthesis
-Mode of transport
–> for the x3 hormone classes (protein/peptide & steroid & amine)?

A
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21
Q

How do peptide/protein hormones activate target cells?

A
  1. Bind to cell surface recs
    –> these act via 2nd messenger
  2. = causes rapid changes in biochem activity
  3. = causing release of STORED (in vesicles) compounds & alteration of gene transcription (LH, FSH, GnRH)
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22
Q

How do steroid hormones activate target cells?

A
  1. Diffuse through cell memb
  2. Bind to cytoplasmic OR nuclear recs
  3. These recs act on TFs
  4. These TFs alter gene expression (testosterone, oestrogen)
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23
Q

Name some of the cell surface receptors that peptide/protein & steroid hormones can bind to.

A

-Gi(-linked?)
-Gq-linked
-Receptor dimerisation

24
Q

How is plasma hormone concentration mainly regulated?

A

-ve feedback

25
Q

What is -ve feedback - in terms of hormones?

A

Level of hormone increases - causes decrease in secretion

26
Q

Examples of hormones regulated by -ve feedback?

A

= Oestrogen, LH & FSH
-Oestrogen inhibits FSH
-Follicle becomes corpus luteum - produces oestrogen & progesterone - inhibit FSH & LH

27
Q

How do -ve feedback mechanisms regulate hormone levels - x2 ways?

A

-Target cell sensitivity = altered
-Level of hormone secreted = altered

28
Q

How can target cell sensitivity or responsiveness (a method -ve feedback mechanisms can use) be used - 2 ways?

A

-Change rec affinity for ligand / change rec activity
-Change no. of recs

29
Q

How does rec affinity / change rec activity -> control target sensitivity - what does it involve doing?

A

-Covalent modification of rec
-Action of inhibitors on rec
-Action of inhibitors on signalling molecule/ligand

30
Q

How can changing no. of recs -> control target sensitivity - what does it involve?

A

-Dec no. recs = will dec sensitivity
-Internalisation of GPCR = desensitisation (rec recycled or degraded)

31
Q

Based upon changing no. of recs to control target sensitivity –> why is pulsatile GnRH secretion required to stimulate LH & FSH?

A

-Long term exposure to constant stimulus abolishes target response to it
-Cells respond to changes in stimulus - rather than quantity

32
Q

What are the gonads in females?

A

Ovaries -> including oocytes & follicles

33
Q

What are the gonads in males?

A

Testes -> including Sertoli cells, Leydig cells, spermatogonia stem cells & seminiferous tubules

34
Q

Internal genitalia of females?

A

-Oviducts
-Uterus
-Cervix
-Upper vagina

35
Q

Internal genitalia of males?

A

-Epididymis
-Vas deferens
-Seminal vesicles

36
Q

External genitalia of females?

A

-Labia minora
-Labia majora
-Clitoris

37
Q

External genitalia in males?

A

-Penis shaft
-Scrotum
-Glans penis

38
Q

Summarise gonads, int & ext genitalia in males & females?

A
39
Q

What do the gonads (m & f) develop from embryologically?

A

Genital ridge - which develops on back wall of embryo @ weeks 6-7

40
Q

How does the genital ridge become a specific gender - i.e., how do some people become males & others females?

A

-Males have SRY gene (on Y chromosome)
= master switching gene
-SRY produces/expresses TDF
–> causes somatic cells of genital ridge to become testis

-Absence of SRY gene - causes ovaries to develop

–> so we are all programmed to become females unless SRY gene changes this

41
Q

Describe male & female sex development.

A

Males
-Possess SRY gene (on Y chromosome)
-SRY gene synthesises TDF -> forms testes
-Testes produces MIH hormone
-MIH causes degeneration of Mullerian ducts (female organs)
-Testis produces testosterone - promotes development of Wolffian ducts (male sex organs)
-Wolffian ducts form male internal genitalia
-Testosterone converted to DHT (by 5-alpha reductase)
-DHT forms male external genitalia

Females
-Do not possess SRY gene (no Y chromosome)
-So do not produce TDF - so ovaries will form
-No testosterone - so Wolffian ducts obliterated
-No testosterone - so no DHT - so female external genitalia forms
-So MIF not produced - so Mullerian ducts are maintained (female organs)
-Mullerian ducts go on to form female internal genitalia

42
Q

What is androgen insensitivity syndrome (AIS)?

A

-X-linked recessive condition
-Affects XY (male) genotype
-Functional SRY gene -> forms testes -> testes produce testosterone & MIH
-However these individuals do not respond to testosterone -> because of an inactivating genetic mutation in androgen rec (AR) gene
= causing dec. testosterone signalling in target cells

-As testosterone is responsible for development of male sex characteristics –> female sex characteristics develop in its absence
-Do not develop external male genitalia (despite having internal testes)
-Develop female sex characteristics (e.g., enlarged breasts)
–> so are genetically male (XY) - but physically resemble females

Complete AIS = look like females (have female ext. genitalia) but have male internal genitalia
-So no uterus, ovaries - do not menstruate

AIS ==> due to mutations in androgen receptor (AR) that completely or partially abolish the androgenic effects of testosterone (T) & dihydrotestosterone (DHT) on androgen-dependent tissues during fetal life & puberty

Partial AIS = testosterone has some effect on sexual development, so genitals often not as expected for boys or girls —> have predominantly female, predominantly male, or ambiguous external genitalia

43
Q

What is congenital adrenal hyperplasia (CAH)?

A

-Autosomal recessive disorders
-Affects XX (female) genotype
-Have ovaries & uterus
-BUT - have external male genitalia

-Cholesterol is converted to aldosterone, cortisol & testosterone
–> conversion to aldosterone & cortisol requires 21-hydroxylase enzyme
–> however in CAH - there is a 21-hydroxylase deficiency - due to a mutation in the 21-hydroxylase gene

-Deficiency in 21-hydroxylase
= dec. aldosterone & cortisol levels - BUT inc in androgens (sex hormones)
–> inc occurs because of accumulation of precursors to the blocked enzymatic step
–> inc. in the precursor 17-hydroxyprogesterone - increases testosterone & DHT -> forms partial male external genitalia

-Dec. aldosterone = loss of Na+, H2O & gain of K+ (salt wasting) -> causing hypotension
-Inc. androgens (sex hormones) = ambiguous female genitalia/male precocious puberty (before age 9)
–> elevated androgens levels affect hypothalamic-pituitary-gonadal axis & sometimes the ovary - causing chronic anovulation & infertility

-Chronic overstimulation of the adrenal cortex = hyperplasia - adrenals grow in size

44
Q

What is Guevedoces?

A

-Autosomal recessive condition
-Affects XY (male) genotype
-5-alpha reductase deficiency - due to genetic mutation to 5-alpha red gene
–> so testosterone cannot be converted to DHT (as requires 5-alpha red)
–> so no DHT -> so no male ext. genitalia

-Female-looking ext genitalia + pseudovagina
-Gonads & int genital organs = male

-@ puberty -> functional penis & typical male secondary sexual features develop

45
Q

What is puberty?

A

-Sexual maturity & fertility
-Physical (secondary sexual features, growth spurt) & beh changes
-Definitive signs of puberty:
*Menarche in girls
*1st ejaculation in boys
–> not immediately signs of fertility

46
Q

How does puberty start?

A

-Before puberty (in childhood) - regulatory synaptic inputs to GnRH-secreting neurons = inhibits GnRH secretion from hypothalamus

  1. Nutritional status (via leptin) = linked to puberty onset
  2. Leptin binds to LepR
  3. = activates Kiss1 neurons (which synapse onto GnRH-secreting neurons)
  4. = increases Kisspeptin signalling
  5. = activates GnRH-secreting neurons
  6. = increases GnRH secretion from hypothalamus
  7. GnRH acts on anterior pituitary
  8. = causes gonadotropin release (FSH & LH)
  9. FSH & LH act on gonads = inc in sex steroids
47
Q

What do gametes originate from?

A

Primordial germ cells (PGCs)

48
Q

What happens to these primordial germ cells?

A

-Remain in quiescent, partially-differentiated state (arrested in metaphase II) until puberty
-@ puberty - oogenesis & spermatogenesis happen for 1st time

49
Q

Function of LH in males?

A

LH stimulates Leydig (interstitial) cells to make testosterone - leading to:
-Spermatogenesis
-Develop/maintain secondary sexual features
-Support secretory activity of accessory sex glands (prostate, seminal vesicles, epididymis)

50
Q

Function of FSH in males?

A

FSH stimulates Sertoli cells to produce:
-Estradiol (type of oestrogen)
-Androgen-binding protein
-Inhibin
-Growth factors needed for spermatogenesis

51
Q

Sperm development - spermatogenesis?

A

-Prior to puberty - prospermatogonia = quiescent (limited mitotic prolif)
-@ puberty - spermatogonia start mitotic division
–> spermatogenesis takes ~64 days (humans)

Stages of permatogenesis:
-Prospermatogonia -> spermatogonium A -> primary spermatocytes -> secondary spermatocytes -> spermatids -> mature sperm (spermatozoa)

52
Q

Function of LH & FSH in females?

A

-LH & FSH -> needed for follicle maturation & ovulation of oocyte (oogenesis)
-LH & FSH contribute to oestrogen & progesterone secretion (= complex pattern)
*FSH stimulates inc oes?
*LH stimulates inc prog?

53
Q

How do growth spurts occur in puberty?

A

-Elevated sex steroid concs (especially oestrogens) stimulate GH production
-Leads to activation of GH/IGF-1 axis
–> where GH is produced by pituitary
–> GH sent to liver (binds to liver?)
–> stimulates IGF-1 (hormone) secretion from liver
-IGF-1 stimulates growth of body during puberty (see image!!!)

54
Q

How do secondary sexual characteristics develop in females & males (during puberty)?

A

Due to action of oestrogens (female) or androgens (male)

55
Q

Effect of testosterone on behaviour?

A

-Testosterone = important for development & maintenance of male sexual behaviour & other factors are crucial (e.g. learning, social interactions, biological)

56
Q

Effect of menstrual cycle on sexual behaviour?

A

-Increase in intercourse frequency & desire around ovulation

-Two main possible causes:
*↑ female libido and sexual behaviour
*↑ women’s sexual attractiveness to males

-BUT other factors are involved (e.g. personal motivation, past experiences, cultural & social factors) as ovarectomy does not cause loss of libido

Endocrinology (2 decks)

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