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PHA223 > sex hormones 1-2 > Flashcards

sex hormones 1-2 Flashcards

1
Q

What type of hormones are all sex hormones?

A

steroid hormones

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2
Q

What are sex hormones synthesised from?

A

cholesterol

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3
Q

What are the male sex hormones called?

A

androgens

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4
Q

main male sex hormone

A

testosterone

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5
Q

What produces testosterone and other androgens?

A

Leydig cells of the testes

adrenal gland (lesser extent)

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6
Q

What are male sex hormones responsible for?

A

foetal differentiation
development of male urogenetial system
some effects on the brain

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7
Q

What happens to Leydig cells after birth?

A

they become inactive until activated by gonadotropins during puberty

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8
Q

What happens during male puberty?

A

androgens cause the sex organs to grow and secondary sex characteristics to develop

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9
Q

explain the release of male sex hormones

A
  • hypothalamus secretes GnRH
  • GnRH causes the anterior pituitary to release FSH and LH
  • FSH acts on sertoli cells and stimulates spermatogenesis and releases inhibin
  • LH acts on Leydig cells and stimulates testosterone secretion
  • testosterone also acts on sertoli cells
  • T acts on hypothalamus and anterior pituitary to inhibit LH and GnRH release
  • Inhibin acts on the anterior pituitary to inhibit FSH release
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10
Q

effects of testosterone

A
  • initiation and maintenance of spermatogenesis
  • decreased GnRH secretion via hypothalamus
  • inhibits LH secretion (anterior pituitary)
  • differentiation of male accessory reproductive organs and maintains their function
  • induces male secondary sex characteristics (opposes oestrogen)
  • protein anabolism, bone growth, cessation of bone growth
  • sex drive
  • aggressive behaviour
  • stimulates erythropoietin secretion by kidneys
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11
Q

2 female sex hormones

A

oestrogen

progesterone

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12
Q

What produces oestrogen and progesterone?

A

ovaries

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13
Q

actions of female sex hormones

A

sexual maturtion at puberty, secondary sex characteristics
control menstrual cycle
higher level during pregnancy by placenta (inhibit ovulation)

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14
Q

How often are female hormones produced?

A

cyclically

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15
Q

effects of oestrogen

A
  • growth of ovary and follicles
  • growth of SM
  • proliferation of epithelial lining of reproductive tract
  • external genitalia growth (puberty)
  • breast growth
  • body configuration (fat distribution)
  • fluid secretion from lipid skin glands
  • bone growth and cessation of bone growth (protects against OP)
  • vascular effects (hot flushes)
  • feedback on hypothalamus and anterior pituitary
  • prolactin secretion
  • protects against atherosclerosis
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16
Q

effects of progesterone

A
  • converts endometrium to secreting tissue suitable for implantation
  • induces thick, sticky cervical mucus
  • decreases contraction of fallopian tubes and myometrium
  • decreases proliferation of vaginal epitheliel cells
  • stimulates breast growth
  • inhibits milk inducing effects of prolactin
  • feedback on hypothalamus and anterior pituitary
  • inc body temperature (after ovulation)
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17
Q

mechanism of release of female hormones

A
  • hypothalamus secretes GnRH
  • causes anterior pituitary to release FSH and LH
  • FSH causes ovarian follicle to mature and secretes oestrogen
  • this causes the uterine lining to thicken
  • LH triggers ovulation
  • it causes the follicular cells to become corpus luteum which secrete progesterone
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18
Q

What is the menstrual cycle?

A

regular changes in the uterine lining resulting in monthly bleeding

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19
Q

What is menarche?

A

first menstrul peroid

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20
Q

What is menopause?

A

termination of cycle due to normal aging of the ovaries

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21
Q

3 phases of the menstrual cycle

A
  1. menses day 0-7
  2. proliferative phase 7-14
    - increase in oestrogen
    - LH rise before ovulation
  3. secretory phase day 14-28
    - ovulation day 14
    - oestrogen drops just before ovulation
    - progesterone increases
    - temparature increases from day 14: 36.4-36.7 (progesterone inc)

day 28 - O and P fall and endometrium sheds again, new cycle

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22
Q

11 contraception methods

A
  1. coitus interrupts
  2. rhythm method
  3. mechanical barriers
  4. chemical barriers
  5. oral contraceptives
  6. injectable contraceptives
  7. insertable contraceptives
  8. contraceptive implants
  9. transdermal contraceptives
  10. IUD
  11. surgical methods
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23
Q

advantages of COC

A
  • reliable and reversible
  • reduced dysmenorrhoea and menorrhagia
  • reduced PMT
  • less symptomatic fibroids/cysts
  • less benign breast disease
  • reduced risk of ovarian/endometrial cancer
  • reduced risk of pelvic inflammatory disease
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24
Q

different types of COC

A

monophasic
biphasic
triphasic
quadraphasic

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25
Q

monophasic COC

A

fixed amount of oeatrogen and progesterogen in each active tablet

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26
Q

biphasic/triphasic/quadraphasic COC

A

varying amounts of oestrogen and progesterone according to the stage of the cycle

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27
Q

What do the first 7 pills of COC do?

A

inhibit ovulation

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28
Q

What do the 14 pills in the 2nd and 3rd week do in COC?

A

maintain anovulation

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29
Q

2 types of oestrogen

A

ethinyl estradion

mestranol

30
Q

What is mestranol?

A

a prodrug converted in vivo to ethinylestradiol

31
Q

equivalent EE to mestranol

A

50 microg mestranol = 35 microg EE

32
Q

active metabolite of desogestrel

A

etonogestrel

33
Q

1st gen progesterone

A

norethisterone (NET)

34
Q

2nd gen progesterone

A

levonorgestrel (LNG)

35
Q

3rd gen progesterone

A

desogestrel
gestodene
norgestimate

36
Q

MOA of COCs

A
  • oestrogen inhibits secretion of FSH via negative feedback on the anterior pituitary and suppresses developmet of the ovarian follicle
  • progesterone inhibits secretion of LH and prevents ovulation
  • it makes cervical mucus less suitable for sperm passage
  • O and P can alter the endometrium to discorurage implantation
37
Q

How does COCs affect fallopian tube?

A

P inhibits motility

O enhances motility causing abnormal rates of ovum transport

38
Q

common adverse effects of COCs

A
  • weight gain (fluid retention or anabolic effect)
  • mild nausea
  • flushing
  • dizziness
  • depression/irritability
  • skin changes (acne/inc pigmentation)
  • amenorrhoea when stopped
  • Oestrogen COCs dec breast milk production (not during BF)
39
Q

contraindications for COCs

A
  • VTE (or risk)
  • prolonges immobilisation
  • ATE (or risk)
  • stroke/TIA
  • Hx migraine with aura
  • DM with vascular symptoms, severe hypertension (risk of arterial TE)
  • Hx severe hepatic disease
  • Hx liver tumours
  • sex steroid malignancies
  • undiagnosed vaginal bleeding
  • hypersensitivity to API/excipients
40
Q

seroiud COCs side effects

A

abdominal pain - gallstones/clot/pancreatitis
chest pain/SOB/blood - lung clot/MI
headaches - stroke/hpt/migraine
eye problems - stroke/hpt/vascular occlusion
severe leg pain - clot

41
Q

When are POPs advantageous?

A
  • pt can’t take oestrogens (COCs/patch/ring)
  • any age
  • smoker and > 35
    premenstraual symptoms and painful periods
  • can be used in BF
42
Q

MOA of POP

A
  • primarily on cervical mucus, in-hospitable to sperm

- P stops implantation through effect on endometrium and on motility/secretions of fallopian tubes

43
Q

contraindications for POPs

A
  • VTE
  • Hx hepatic disease
  • sex steroid malignancies
  • undiagnosed vaginal bleeding
  • hypersensitivity to API/excipitnts
  • allergy to penut/soya
44
Q

What is ulipristal?

A

orally acive synthetic selective progesterone receptor modulator
acts via high affinity binding to the human progesterone receptor

45
Q

MOA of ulipristal

A

inhibition/delay of ovulation via suppression of the LH surge

46
Q

How does ulipristal work after the LH surge?

A

it delays follicular rupture

47
Q

indications for EHC

A 
UPSI
reduced efficacy of contraception
- torn/leaky condom
- missed pills
- late implant/injection
- detached patch
48
Q

What is menopause?

A
  • when a woman stops menstruating and reached the end of her natural reproductive life
  • when not had period for 12 consecutive months
  • ovaries stop maturing eggs and secreting oestrogen and progesterone
49
Q

definition ofmenopausal women

A

includes women in perimenopause and postmenpause

50
Q

perimanopause

A

time where a woman has irregular cycles of oculation and menstruation leading up to menopause and continuing until 12months after her final period

aka manopausal transition/climacteric

51
Q

postmenopause

A

time after menopause has occurred

starting when a woman hasn’t had a period for 12 consecutive months

52
Q

age of manupause

A

between 45 and 55 years

53
Q

manopause symptoms

A 
hot flushes
vaginal dryness
atrophy of breasts
depression
loss of libido
loss of self esteem
weight gain
54
Q

vasomotor symptoms of menopause

A

hot flushes
night sweats
formication

55
Q

urogenital menopause symptoms

A 
dry vagina
atrophic vaginitis
dyspareunia
local microtrauma
incontinence
56
Q

physical changes with menopause

A

decreased fitness and flexibility
changes in distribution of body fat
changes in sleep patterns

57
Q

What causes hot flushes?

A

oestrogen withdrawal affects the central adrenergic system

causes release of catecholamines and prostaglandins that produce hot flushes

58
Q

hot flush triggers

A 
cigarette smoking
alcohol
caffeine
stress
heat (temp change)
hot spicy foods
exercise (release of catecholamines)
59
Q

lifestyle advice for menopause

A

diet - reduce caffeine, spicy foods, alcohol
exercise
stop smoking
stress relief and relaxation (dec catecholamines and PGs)- yoga
holistic approach

60
Q

When is HRT given for menopause?

A

women who have an intact uterus

61
Q

routes of admin for HRT

A

orally - conjugated oeatrogens, oestradiol, oestriol
vaginally - prssary/cream - oestradiol
transdermal patches - oestradiol
subcutaneous implant - oestradiol

62
Q

metabolism of oral oestrogens

A

undergo first pass metabolism

63
Q

contraception and HRT

A

HRT doesn’t provide contraceptive cover

woman potentially fertile for 2 years if under 50 and for 1 year if over 50

64
Q

risks of HRT

A

increases risk of endometrial/breast/ovarian cancer

oestrogen stimulation causes proliferation of the endometrium inc risk of malignancy

breast cancer - related to duration of therapy, only inc over age 50, higher in women taking combined HRT compared to O only

65
Q

What should be given with oestrogen HRT?

A

progesterone for 14 days of the cycle only

66
Q

hysterectomy

A

removal of uterus

67
Q

What is mirena in situ?

A

LNG-IUS

68
Q

HRT for hysterectomy or mirena in situ

A

oestrogen only

- oral or transdermal gel/patch

69
Q

HRT for NO hysterectomy or mirena in situ

A

oestrogen and progesterone

perimenopausal - sequential therapy
postmenopausal - continuous combined

70
Q

indications for transdermal therapy

A
  • porr symptom control with oral
  • GI disorder affecting oral
  • PMH/FH of VTE
  • BMI > 30
  • variable BP control
  • migraine
  • gall bladder disease
  • hepatic inducing enxyme meds
71
Q

When should testosterone therapy be considered?

A

after bilateral oophorectomy

surgical removal of ovaries

PHA223 (43 decks)

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