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Reproductive system > Lecture 7- HPG axis > Flashcards

Lecture 7- HPG axis Flashcards

1
Q

The Hypothalamus-pituitary-gonadal axis is switched on during

A

puberty

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2
Q

The Hypothalamus-pituitary-gonadal axis involves

A
  • Hypothalamus
  • Pituitary
  • Gonadal glands
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3
Q

examples of hormones produced by the AP

A

(1) prolactin (PRL), (2) growth hormone (GH), (3) adrenocorticotropic hormone (ACTH), (4) luteinizing hormone (LH), (5) follicle-stimulating hormone (FSH), and (6) thyroid-stimulating hormone (TSH)

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4
Q

examples of hormones produced by the PP

A

ADH and oxytocin

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5
Q
  • HPG Axis Regulates the function of:
A
  • The thyroid (hypothalamic-pituitary-thyroid axis HPT)
  • Adrenal (hypothalamic-pituitary- adrenal axis HPA)
  • Reproductive glands (Hypothalamus-pituitary-gonadal axis)
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6
Q

HPG also controls

A
  • Somatic growth
  • Lactation
  • Milk secretion
  • Water metabolism
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7
Q

puberty and HPG

A
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8
Q

pubertry is initiated in the

A

hypothalamus

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9
Q
  • what precedes phenotype changes by several years
A
  • Nocturnal GnRH pulsality (LH secretion) precedes phenotype changes by several year
    • Phenotypic changes (breast buds/testicular enlargement seen)
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10
Q
  • Onset of puberty associated with steady rise in
A

FSH and LH secretion

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11
Q

why is precocious puberty- early onset- rare

A
  • Not common because hormone levels low
  • Due to low GnRH secretion
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12
Q

GnRH

A
  • Production occurs in the neurones of the hypothalamus and causes downstream production of sex hormones by the gonads
  • Regulates puberty onset, sexual development and ovulatory cycles in females
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13
Q
  • Intrinsic or extrinsic disruption to GnRH production can lead to development of
A

pathologic conditions in humans

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14
Q
  • Pharmacologic analogs of GnRH are useful in the treatment of
A

gynaecological disease due to their ability to block oestrogen and progesterone secretion from the ovary

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15
Q
  • Location of the GnRH receptor in the
A
  • Location of the GnRH receptor in the anterior pituitary and is a GPCR
    • When bound by an activating subunit, undergo conformation change and activate in intracellular pathways leading to modulation of genes within a target cell via phosphorylation events
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16
Q
  • At birth the GnRH neurones are
A

complete, but functional maturation of synaptic connectivity is attained especially at puberty

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17
Q

GnRh release in early puberty

A
  • Initially at puberty, GnRH is released in low-frequency but after maturation of synaptic connections, it matches male pattern
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18
Q

GnRh secretion in males

A

GnRH pulses occur after 2 hours

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19
Q
  • GnRH secretion in females,
A

changes according to phases in menstrual cycle

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20
Q

GnRH-1 gene

A

primarily responsible for mammalian GnRH

  • exclusively expressed in discrete popualtion of neurones int he hypothalamus
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21
Q

if GnRH production is blocked

A

lack of gonadotrophin synthesis and secretion and therefore alck of reproductive development

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22
Q

artifical administration of GnRH can

A

induce spermatogensis and ovarian maturation

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23
Q

Artificial administration to drive fertility must be

A

pulsatile in humans- constant admin causes desensitisation of cells in anterior pituitary glands

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24
Q

Anterior pituitary (adenohypophysis)

A
  • Glandular
  • Anterior lobe that together with the posterior lobe (neurohypophysis) makes up the pituitary gland (hypophysis)
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25
Q
  • Secretion of GnRH by hypothalamus stimulates the anterior pituitary gland gonadotrophs
    *
A
  • FSH
  • LH
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26
Q
  • GnRH release is pulsatile (every 1-3 hrs)
  • Intensity of GnRH stimulus is affected by
    *
A
  • Frequency of release
  • Intensity of release
27
Q

GnRH travels to pituitary in

A

hypophysial portal system

28
Q

In young children, LH and FSH levels are insufficient to initiate

A

gonadal function

29
Q

between which ages does blood levels fo LHa nd FSH increase

A

9-12

30
Q
  • Amplitude of LH and FSH pulses increases esp
A

during sleep

31
Q

high levels of LH and FSH

A
  • High levels of LH, FSH initiate gonadal development
32
Q
A
33
Q

Sleep dependent rise in nocturnal LH

A
  • In adolescents boys the sleep related LH increase
  • Stimulates a nocturnal rise of testosterone
  • Androgen level increase account for some of the early pubertal changes seen in male
  • Similar pattern in females with concomitant increase in oestrogen
34
Q

negatiev feedback look of HPG

A
  • Negative feedback will dampen hypothalamic release of GnRH
    • High levels of androgens and oestrogen will give negative feedback to the hypothalamus
  • To prevent constant release of GnRH- due to desensitisation of receptors in the pituitary
35
Q
A
36
Q

LH in males

A
  • stimulates Leydig cells in testis to produce testosterone (steroid hormone- cholesterol)
  • Once production starts in the medium long-term testosterone levels remain constant
  • There is an effect on:
    • Circadian rhythm
    • Highest early morning
    • Effects of environmental stimuli
    • Both driven by brain
37
Q

FSH in males

A
  • FSH stimulates Sertoli cells
    • Spermatogenesis
    • Inhibin release- negative feedback on anterior pituitary and possibly hypothalamus
38
Q

Role of testes

  • *
A
  • Each lobule contains 1-4 tightly coiled seminiferous tubules
  • Each ST -60cm long
    • 90% of testicular volume
    • Location of spermatogenesis
  • In between there is loose connective tissue and blood vessels
    • Interstitial tissue contains Leydig cells
39
Q

Seminiferous tubule cells

*

A
  • Line by complex epithelium made up of 2 types of cells
    • Supporting cells (Sertoli cells)
      • Provide nutrition and hormonal support for germ cells
      • Sensitive to FSH – increase sperm production
      • Secrete inhibin- negative feedback on AP FSH
    • Spermatogenic cells
40
Q

FSH in females

A
  • Granulosa cells convert androgen to oestrogen
  • Follicular development
    • Releases inhibin
    • Specifically inhibits FSH
41
Q

Inhibin in women speficifically inhibits

A

FSH (not LH)

42
Q

LH in females

A
  • LH stimulates theca interna cells
    • Release androgens- converted to oestrogen by granulosa cells
    • LH surge require for ovulation
    • LH maintains corpus luteum after ovulation.
      • Releases progesterone and oestrogen
      • Last 12-14 days unless further stimulated by pregnancy hormone beta hCG (released after implantation
43
Q
  • Moderate titres of oestrogen and GnRH secretion
A
  • Moderate titres of oestrogen reduce GnRH secretion
    • Negative feedback
    • Progesterone increases inhibitory effects of moderate oestrogen
44
Q
  • High titres of oestrogen and GnRH
A
  • High titres of oestrogen alone promotoe GnRH secretion
    • Positive feedback
    • LH surge- ovulation
    • Progesterone prevent positive feedback of high oestrogen
45
Q

oestrogen reduces GnRH by

A

pulse

46
Q
  • Progesterone reduces GnRH by
A

frequency of pulses

47
Q
  • Inhibin on FSH
A
  • Secreted from granulosa cells
  • Inhibits secretion of FSH (same as male)
  • Has small inhibitory effect on LH
48
Q

summary of the hormonal feedback loop

A
49
Q

hormonal changes in puberty

A
  • increased TSH
  • increased metabolic rate
  • promotes tissue growth
  • increased androgens= retention of mineals in body to support bone and muscle growth–> leadin to growth sput
50
Q

The role of leptin

*

A
  • An adipocyte- derived protein hormone
  • Signals info about energy store to CNS
    • Important role in regulating neuroendocrine function
    • Reproductive dysfunction associated with leptin deficiency
    • Leptin can accelerate the onset of repro function
51
Q
  • Leptin has ……. release pattern signif associated with variations in LH
A
  • Leptin has pulsatile release pattern signif associated with variations in LH
    • Leptin can regulate GnRH levels and its secretion may, in turn, be influenced by gonadal steroids but appears to be independent of LH control
52
Q

percocious puberty can be

A

central or peripheral

53
Q

Central precocious puberty

A

Precocious puberty with elevated GnRH levels (due to hypothalamus)

54
Q

cause sof central precocious puberty

A
  • Idiopathic or constitutional
  • CNS lesion
  • Pituitary gonadotropin-secreting tumours
  • Systemic conditions- tuberous sclerosis, neurofibromatosis
  • Obesity- levels of leptin
55
Q

pathophysiology of central precocious puberty

A
  • Premature activation of the hypothalamus-hypophyseal axis–> abnormally early initiation of pubertal changes–> early development of secondary sexual characteristics and gonadarche
56
Q
  • Diagnosis- lab tests
A
  • Basal LH and FSH= increased
  • GnRH stimulation test (gold standard): gonadotropin (LH and FSH) levels increase after intravenous admin of GnRH
  • increased testosterone and oestrogen
57
Q

Peripheral precocious puberty

A

Precocious puberty without elevated GnRH levels (not a problem with the hypothalamus)

58
Q

causes of peripheral precocious piberty

A
  • icnreased androgen production
    • ovarian cyst (most common)
    • congentiala drneal hyperplasia
    • Virilizing ovarian and adrenocortical tumours
    • leydig-cell tumour
  • Increased oestrogen
    • HCG- secreting germ cell tumours e.g. granulosa cell tumour
    • rarely: adrenal gland tumors that produce oestrogen
    • McCunes-albright syndrome
  • icnreased B-HCG production e.g. hepatoblastoma
  • primary hypothydroism
  • obestiy related precoous sexual development due to compensatory hyperinsulinemia
59
Q

lab tests for Peripheral precocious puberty

A
  • icnreased oestrogen or testosterone
  • decreased LH and FASH (GnRH suppressed by eleavted gonadal hormones)
60
Q

Delayed onset of puberty

A

Absent or incomplete development of secondary sex characteristics by the age of 14 or 13 in girls

61
Q

causes of Delayed onset of puberty

A
  • constitutional growth delay (most common cause of delayed puberty)
  • malnutrition and other chronic diseases e.g. IBD, hypothyrodism, psychosocial deprivation
  • hypogonadism
62
Q

constitutional growth delay

A

a temporary delay in growth and osnet of puberty that is not caused by a pathological process

e. g. inherited autosomal dominant, recessive, or X-lined trait
diagnosis: X ray showing bone age that is less than the individuals chronological age
treatment: no treatment is needed, as catch-up growth eventually occurs and the individual reaches normal height

63
Q

Delayed onset of puberty lab test

A

basal LH and FSh

Reproductive system (28 decks)

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