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The Patient > Sex hormones > Flashcards

Sex hormones Flashcards

1
Q

What links testosterone and oestrogen?

A

androstenedione (testosterone precursor) is also a precursor to estrone via aromatase. both estrone and testosterone can be converted to estradiol.

testosterone -> estradiol also via aromatase

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2
Q

What is DHT?

A

dihydrotestosterone - a stronger angroden

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3
Q

Role of oestrogen in males?

A

still important - circulate at about 20% of the concentration in non pregnant females

thought to be important after puberty in sustaining spermatogenesis

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4
Q

Main features of the male reproductive tract?

A
  • bladder, prostate (surrounds urethra)
  • vas deferens
  • epididymis
  • testes
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5
Q

Functions of the testes?

A

sperm production, steroid hormone production

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6
Q

Function of the epididymis?

A

sperm collection and maturation

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7
Q

Function of the ductus deferens?

A

transport and storage

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8
Q

Structure of the testes?

A

Semineferous tubules - sperm production

Epididymis - sperm maturation

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9
Q

What are sertoli cells?

A

cells in the semineferous tubules, allow progression of germ cells to sperm cells

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10
Q

Which cells produce testosterone?

A

Leydig cells

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11
Q

In which cells does the testosterone to DHT conversion take place?

A

Sertoli cells

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12
Q

What is the nuclear receptor superfamily?

A
  • receptors for all major classes of steroid hormone
  • proteins that have two binding sites: one for the steroid and one for DNA
  • binding of the steroid produces a complex that acts on DNA
  • binding of the complex alters the repetoire of genes being expressed
  • this activity defines steroid receptors as transcription factors
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13
Q

What is the androgen receptor?

A
  • androgens are defined as compounds that act on the androgen receptor
  • all major cell populations in the testes, epididymis and accessory glands express these receptors
  • the cell types require androgen binding to fulfil their roles
  • also found in tissues where secondary sexual characteristics appear
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14
Q

What is the HPG axis?

A
  • hypothalamus releases GnRH
  • A. pituitary releases gonadotrophins (LH and FSH)
  • gonadotrophins control sex steroid production
  • sex steroids control production of sperm/maturation
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15
Q

Action of FSH on the testes?

A

Binds to sertoli cells to convert testosterone to DHT

this then stimulates the rest of the process (spermatogenesis etc)

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16
Q

Feedback control of sex hormones in males?

A

Testosterone inhibits secretion of gonadotrophins and GnRH, inhibin also inhibits secretion of gonadotrophins

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17
Q

Why do men not have a monthly cycle of sex hormones?

A

No positive feedback regulation

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18
Q

Action of LH on the testes?

A

binds to Leydig cells to synthesise testosterone, which is then transported to sertoli cells

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19
Q

What is the function of the Myoid cells?

A

muscular - contract to move sperm along semineferous tubule. action is androgen dependent

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20
Q

Can the sperm swim when they leave the tubules?

A

No, this is acquired in the epididymis (DHT dependent)

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21
Q

Average volume of ejaculate?

A

1.5-5mL

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22
Q

Average sperm count?

A

40-250 million/mL

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23
Q

Composition of ejaculate?

A

Epididymis and ductus deferens secretion (sperm rich): 5%
Prostatic secretion: 13-33%
Seminal vesicle secretion: 46-80%
Bulbo-urethral gland secretion: 5%

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24
Q

Definition of erection?

A

Erectile tissue becomes engorged with blood, arterioles dilated as a result of parasympathetic nervous system activity

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25
Q

What is emission/ejaculation controlled by?

A

Sympathetic nervous system

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26
Q

Pathologic bases for erectile dysfunction?

A

psychogenic; neurogenic; vascular and endocrine

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27
Q

Latrogenic causes of impotence?

A

many drugs including tricyclics and SSRIs ; antihypertensives including beta blockers and calcium antagonists

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28
Q

Prevalence of prostate cancer?

A
  • second leading caues of cancer death after lung
  • overall lifetime risk 1 in 6
  • risk factors: age, ethinicity, family history
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29
Q

Symptoms of prostate cancer?

A
  • frequent/urgent urination
  • nocturnal enuresis (involuntary urination)
  • difficulty starting or emptying bladder
  • urine flow weak, interrupted or difficult to control
  • back or pelvic pain
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30
Q

Pharmacological management options for prostate cancer?

A

GnRH agonists and antagonists
Androgen antagonist - cyrproterone acetate
5-a-reductase inhibitors, dutasteride and finasteride

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31
Q

Clinical uses of anabolic steroids?

A

treatment of some aplastic anaemias

  • protein building properties have not proved beneficial in a clinical setting
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32
Q

How would male contraception work?

A

Exogeneous testosterone: inhibit FSH and LH

would need high doses as difficult to decrease sperm count

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33
Q

What is Testosterone undecanoate ?

A

longer acting testosterone depot, better PK

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34
Q

Alternative possibility for male contraception?

A

Reversible Inhibition of Sperm Under Guidance

‘Vasalgel’ - gel injected into vas deferens, sperm cannot penetrate and are reabsorbed

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35
Q

Approx how many menstrual cycles do women have?

A

468

36
Q

Name of the stage of menstrual cycle days 1-5?

A

menses

37
Q

Name of the stage of menstrual cycle days 5-14?

A

ovary: follicular
endometrium: proliferative

38
Q

Name of the stage of menstrual cycle days 14-28?

A

ovary: luteal
endometrium: secretory

39
Q

What is the HPO axis?

A
  • hypothalamus releases GnRH
  • A pituitary releases gonadotrophins (FSH and LH)
  • gonadotrophins control both sex steroid production and follicle maturation/ovulation in the ovary
40
Q

Structure of GnRH?

A

10 amino acids

acts at GnRH receptor (a GPCR)

41
Q

What is the significance of how GnRH is released?

A

pulsatile. FSH is stimulated by slow pulse frequencies, LH stimulated by faster ones

42
Q

What are GnRH agonists and antagonists used for in females?

A

‘shut down’ the ovary before a controlled cycle of stimulation

43
Q

Example of a GnRH agonist?

A 
Buserelin. stimulates FSH and LH production
long term effects:
- GnRH receptor down-regulation
- resulting GnRH insensitivity
- loss of FSH and LH production
44
Q

How does rising fat levels in girls trigger puberty?

A

rising fat levels triggers leptin release

leptin stimulates kisspeptin neurone, which acts on the GnRH neurone

45
Q

Risks associated with early puberty?

A

higher chance of type 2 diabetes and CVD

46
Q

Risks associated with late puberty?

A

Higher risk of osteoporosis, but lower risk for breast cancer

47
Q

What happens in the ovarian cycle?

A

follicular development, then LH causes ovulation

corpus luteum forms then degrades

48
Q

Hormone patterns throughout menstrual cycle?

A
  • low oestrogen and progesterone levels stimulates release of FSH
  • FSH triggers release of oestrogen
  • Oestrogen triggers sharp release of LH (positive feedback for ovulation) (+ negative feedback on FSH)
  • corpus luteum then secretes oestrogen and progesterone, which inhibits FSH and LH
  • if no fertilisation, corpus luteum degrades, O+P fall and begins again
49
Q

What inhibits GnRH?

A

Progesterone and oestrogen, or prolonged high oestrogen alone

50
Q

What else does oestrogen do?

A

Stimulate growth of endometrium (DNA synthesis)

51
Q

HOw do anti-oestrogens work?

A

bind to the oestrogen receptor, induces a conformational change in the receptor so cant bind to DNA

52
Q

Mechanism of tamoxifen?

A

Partial agonist and partial antoagonist

53
Q

Some of the positive effects of oestrogen?

A
  • preserve bone density
  • regulation of cholesterol production
  • maturation of ovary and uterus
  • menstrual regulation
  • vaginal maintenance
54
Q

Some of the negative effects of oestrogen?

A
  • exposure can increase risk of breast cancer

- exposure may increase risk of uterine cancer

55
Q

Definition of menopause?

A

permanent cessation of ovarian activity usually said to have occurred after 12 consecutive months of amenorrhoea

56
Q

Definition of perimenopause?

A

period before menopause and 1st year after it

57
Q

Climacteric?

A

transition from reproductive life to non-reproductive state

58
Q

How does menopause affect life expectancy?

A

reduced 2% with each increasing year beefore reaching menopause
ischaemic heart disease 2% lower
risk of death from uterine or ovarian cancer increased by 5%

59
Q

Effects of oestrogen withdrawal on other organs?

A
  • vasomotor symptoms (flushing)
  • dyspareunia (ainful sex)
  • more UTIs
  • improved depression scores
  • slower wound healing
  • more inflammation
  • decreased bone density
60
Q

Dose required to stimulate vagina and lower urethra?

A

10mcg/day

61
Q

What is menstruation?

A

shedding of the superficial layer of the uterus

62
Q

How does withdrawal of sex steroid support induce menstruation?

A

vasoconstriction, hypoxia, connective tissue breakdown, fragmentation

coagulation factors control blood loss locally

63
Q

Where does fertilisation normally occur?

A

Upper fallopian tube

64
Q

What is the pre-implantation stage?

A
  • 30 hours of cleavage to the 8 cell stage
  • Morula at 72 hours
  • Blastocyst at4 days
  • Implanted blastocyst at 6 days
65
Q

What stage must fertilised cells reach in order to implant?

A

blastocyst

66
Q

Where in the endometrium does the blastocyst implant?

A

interstitial - underneath the endometrium surface

67
Q

What is the implantation window for a fertilised egg?

A

7-10 days post ovulation - corpus luteum cant sustain any longer

68
Q

What is hCG?

A

Human chorionic gonadotrophin

  • polypeptide, produced by the placenta
  • use dfor pregnancy testing as appears in blood and urine soon after inplantation
  • rescues the corpus luteum
  • lack of hCG appearance probably accounts for the closure of the implantation window
69
Q

How do hCG, progesterone and oestrogen levels change throughout pregnancy?

A
  • hCG spikes at about 10 weeks, then declines again to basal level, then increases slightly again at 36 weeks
  • oestrogen and progesterone increase steadily, p. tapers off slightly towards the end
70
Q

Functions of progesterone during pregnancy?

A
  • regulates the rate of transport of the egg/embryo through the Fallopian tube
  • prepares the uterus to receive the implanting blastocyst
  • sustains the uterine lining (endometrium) throughout pregnancy
  • inhibits myometrial contractility
71
Q

what is the luteoplacental endocrine switch?

A

placenta takes over secretion of progesterone and oestrogen from CL at 7-9 weeks

72
Q

How are androgens/testosterone produced during pregnancy?

A

progesterone -> androgens in the fetus, then androgens to oestrogen in the mother

73
Q

When is a pregnancy described as viable?

A

when heartbeat can be seen within gestational sac

  • 5 weeks LMP vaginally
  • 6 weeks abdo
74
Q

Possible locations for ectopic pregnancy?

A
  • fimbrium/infundibulum
  • interstitial
  • ovarian
  • broad ligament
  • ampulla
  • isthmic
  • abdominal
  • cervical
75
Q

Signs/management of ectopic pregnancy?

A
  • abdominal pain
  • hCG detected
  • scan - no intrauterine body
  • tube rupture can be fatal
  • medical management or surgery?
  • methotrexate
76
Q

When can pregnancy termination be carried out?

A

up to 24 weeks, most are done before 13

77
Q

What is mifepristone?

A
  • antagonist at progesterone receptor
  • counteracts effects of progesterone on pregnancy: blocks preparation of the endometrium for pregnancy
    and counteracts the suppressive effect of P on myometrial contractility

can also be usedas contraception but not widely used

78
Q

How is medical termination carried out?

A

mifepristone, followed by prostaglandin to initiate contractions

79
Q

What is human placental lactogen

A

modulates intermediary metabolism by changing the level of insulin-like growth factor (IGF) - increases glucose and amino acid availability to the fetus

80
Q

Key stages of human pregnancy?

A
  • gestation 38 weeks
  • 3 trimesters
  • embryonic up to 10 weeks, formation of major organs
  • fetal after 10 weeks, maturation, develpoment and growth
81
Q

Hormonal control of labour?

A
  • progesterone prevents contractility
  • initiation of labour may be through inflammatory mediators
  • stimulation with oxytocin, prostaglandins and thromboxane
82
Q

Why is glucocorticoid treatment used in some pregnancies?

A

Mature the fetal lungs for early delivery

83
Q

Which drugs are most likely to cross the placenta?

A

lipophilic (unionised), weakly basic

larger e.g. heparin negligible

84
Q

What is Fetal Valproate syndrome?

A

birth defects, lifelong alterations to behaviour and development

85
Q

Definition of preterm labour?

A 
<37 weeks
approx 5-10% of births are preterm
- parental distress
- expensive neonatal intensive care
- some deaths
- long term morbidity
86
Q

Treatments that can help prolong pregnancy in early labour?

A

Ritodrine (beta agonist), Atosiban (oxytocin antagonist), Nifedipine (calcium channel blocker)

87
Q

cautions for drug use in pregnancy?

A
  • try to avoid all drugs in 1st
  • taper to lower effective dose for essential therapy before conception
  • if appropriate, switch to a safer one

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