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1. See discussions, stats, and author profiles for this publication at: https://www.researchgate.net/publication/294579673
FEMALE SEX HORMONES
Presentation · January 2016
DOI: 10.13140/RG.2.1.4255.4647
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3. Ovarian Hormones
Introduction:
Menstrual cycle: it reflects the
functional activities of the ovary,
starts at puberty and continues
throughout about 30 to 40 years in
a cyclic manner with episodes of
regular bleeding.
4. Menopause: cessation of
menstrual cycles due to failure of
the ovary to respond to the
gonadotropins secreted by the
anterior pituitary gland at a mean
age of 52 years.
5. The onset of menstrual cycles may
be due to neural mechanism:
- Amygdala of the brain
withdraws its inhibition on the cells
of the median eminence of the
hypothalamus (maturation centers)
produce gonadotropin-
releasing hormone (GnRH)
stimulates the pituitary to release
follicle-stimulating hormone (FSH)
and luteinizing hormone (LH)
stimulate ovary to function.
7. FSH and LH are secreted first in
small amounts small quantity of
estrogen is produced breast
development, alteration of fat
distribution, growth spurt and later
epiphysial closure.
After about one year later
sufficient amount of estrogen is
produced endometrial changes
and periodic bleeding.
The first few cycles are anovulatory
8. Sequence of events in menstrual
cycles:
At the beginning of each cycle FSH
causes enlargement of variable
number of follicles (vesicular follicles)
each containing an ovum.
After 5 to 6 days one follicle begins
to develop more rapidly.
Under the influence of LH
multiplication of granulosa cells of the
rapidly growing follicle synthesis
and release of increasing amounts of
estrogens inhibition of FSH release
regression of the other smaller and
less mature follicles.
9. The structure of this mature
follicle is an ovum surrounded by
a fluid-filled antrum and lined by
granulosa and theca cells.
The peak of estrogen secretion is
reached just before the mid cycle.
At that time the granulosa cells
begin to secrete progesterone.
11. A brief surge of FSH and LH
release rupture of the follicle
release of the ovum (ovulation)
into the peritoneal cavity
picked-up by the fembria of the
fallopian tube.
12. After ovulation the cavity of the
ruptured follicle is filled with blood
(corpus hemorrhagicum) proliferation
of the luteinized theca and granulosa
cells to replace the blood in the cavity
formation of corpus luteum :
Without pregnancy production
of estrogen and progesterone
throughout the reminder of the
cycle degenerates declining
of hormone production corpus
albicans.
With pregnancy production of
estrogen and progesterone but
for a longer period.
13. The associated endometrial changes
include proliferation of endometrial
cells during follicular phase and
development of its glandular structure
during luteal phase the sheds-out
(menstruation) if there is no
pregnancy.
At menopause no estrogen nor
progesterone secretion from the ovary
but small quantities of estrogen may
appear due to conversion of adrenal
and ovarian steroids (e.g.
androstenedione) to esterone and
estradiol mainly in the adipose tissue.
14. The Estrogens:
Types of estrogens:
A- Natural: - Estradiol (major
product of ovary)
- Estrone (E1) from the
ovary but mainly in
liver.
- Estriol (E2) mainly in
liver.
16. In normal women: plasma level of
estradiol in early follicular phase is
50 pg/ml, and 350- 850 pg/ml in the
preovulatory peak.
17. Synthesis and metabolic pathways of
estrogens:
Follicular phase Luteal phase
Prenenolone Prenenolone
17-α-Hydroxypregnenolone Progesterone
Dehydroepiandrosterone 17-α-hydroxyprogesterone
Androsenedione Testosterone
Esterone
16-α-hydroxyesterone
Estriol 17-β-estradiol
2-hydroxyesterone
And other metabolites
2-hydroxyestradiol
And other metabolites
18. Pharmacokinetics:
The released estradiol binds
strongly to α2-globulin (sex
hormone-binding globulin “SHBG”)
and less affinity to albumin
unavailable to enter the target
cells.
Free estradiol is physiologically
active.
19. In the liver and other tissues:
estradiol estrone and estriol
(low affinity to estrogen receptors)
hydroxylation metabolites
lipid insoluble cannot cross the
cell membrane (inactive)
excreted in the bile to intestine
hydrolysis of the conjugated
compounds reabsorption to liver
(enetro-hepatic circulation)
increase synthesis of clotting
factors and plasma renin substrate
undesirable side effects.
20. To avoid the first-pass hepatic
exposure (and undesired side
effects) in postmenopausal women
use injections, transdermal, or
vaginal routes.
Small amounts of estrogens are
excreted in breast milk.
22. Free estrogen enters the cell binds to
receptors (receptor+ heat shock proteins
“Hsp90” complex + other proteins that
stabilize them) conformational changes
dissociation of the receptor-hormone
complex from the Hsp homodimers
(active) transported to the nucleus
binds to estrogen receptor element “ERE”
of the gene & to other sites in the
promoter region of the gene complexes
with nuclear proteins “transcription
elements” regulates transcription by
RNA polymerase II and the transcription
factors mRNA editing of mRNA to
the cytoplasm specific protein
hormone response.
24. Non-nuclear mechanism:
Through specific membrane
receptors rapid effects e.g.
granulosa cell Ca2+ uptake and
increased uterine blood flow.
These hormone receptors differ
from intracellular receptors.
25. II-Female Maturation:
They stimulate the development of
the vagina, uterus, and uterine
tubes.
Stimulate the development of
secondary sexual characteristics.
Stimulate stromal development and
ductal growth of the breast.
26. Responsible for the accelerated
growth phase and closure of the
epiphyses of long bones at
puberty.
Contribute to the growth of axillary
and pubic hair.
Alter distribution of body fat
typical female body contours.
Stimulate pigmentation of skin
especially the nipples, areolae, and
genital region.
27. III-Endometrial effects:
Growth of the uterine muscles.
Development of endometrial lining.
Continuous exposure for a long
period abnormal hyperplasia of
the endometrium abnormal
uterine bleeding.
28. IV-Metabolic effects:
Maintains normal structure of the
skin and blood vessels in women.
Has an antagonizing effects on
parathyroid hormone decreases
the rate of bone resorption.
Reduces the motility of bowel
alters intestinal absorption.
29. circulating level of transcortin (CBG),
thyroxine-binding globulin (TBG), sex
hormone-binding globulin (SHBG),
transferrin, renin substrate, and
fibrinogen increase thyroxine,
estrogen, testosterone, iron, copper,
and other substances.
Increases in high-density lipoproteins,
slight reduction of low-density
lipoproteins, reduction of plasma
cholesterol level, and increase levels of
plasma triglyceride
Decreases oxidation of adipose tissue
lipid to ketones and increases synthesis
of triglycerides.
30. V-Effects on blood coagulation:
Increases circulating levels of
factors II, VII, IX, and X and
decreases antithrombine III
enhance blood coagulability.
Increases plasminogen levels and
decreases platelet adhesiveness.
31. VI-Other physiologic effects:
Synthesis of progesterone receptors.
Responsible for estrous behavior in
animals and influences lipido in
humans.
Facilitates loss of the intravascular fluid
into the extracellular space edema
decrease in plasma volume
compensatory retention of sodium and
water by the kidney.
Modulates sympathetic nervous system
control of smooth muscle function.
33. In primary failure start treatment at
age 11- 13 years to:
a-Stimulate development of secondary
sexual characters.
b-Initiate menstrual cycles.
c-Stimulate optimal growth.
d-Avoid psychological disturbances
consequent of delayed puberty.
Start treatment with small doses of
estrogen on day 1 to day 21 each
month. After optimal growth is
completed administer estrogen and
progestin chronically.
34. B-Postmenopausal Hormonal Therapy:
Manifestations of menopause:
1- Loss of periods.
2- Vasomotor symptoms e.g. hot
flushes.
3- Genital atrophy.
4- Acceleration of bone loss may
lead to vertebral, hip, and wrist
fractures.
5- Lipid changes accelerated raise in
plasma cholesterol and LDL, and
LDL receptors decline
acceleration of cardiovascular
diseases.
35. To control these menopausal
manifestations:
a-Estrogen replacement therapy
improves lipid and lipoprotein
profiles reduction o myocardial
infarction, reduction of fatal
strokes.
b-Control hypertension, diabetes,
and lipid disorders if present.
c-Quit smoking, regular exercise,
and loose weight.
d-Antioxidant vitamins, folic acid,
and aspirin.
36. Optimal management of postmeno-
pausal women: In addition to
lines adopted to control these
manifestations:
For hot flushes, insomnia,
sweating, and atrophic vaginitis
lowest dose of estrogen for a
limited period of time. Estrogen
can be given alone 5 days a week
or continuously.
37. For osteoporosis (this risk is more in:
thin heavy smokers, inactive, with low
calcium intake, strong family history of
osteoporosis) give estrogen on the
first 21- 25 days in each month. Begin
therapy as soon as possible after
menopause to obtain maximum effect.
Supplement with calcium (up to 1500
mg daily). Combine estrogen with
progesterone to prevent endometrial
hyperplasia and reduce the risk of
endometrial cancer ( estrogen for first
25 days and progestin during the last
10-14 days of this period). With this
cyclic therapy usually there is bleeding
at the end of each cycle and migraine
headache.
38. To avoid disadvantages of cyclic
therapy continuous therapy i.e.
daily therapy with 0.625 mg of
conjugated equine estrogens and 2.5-
5 mg medroxyprogesterone will
eliminate cyclic bleeding, control
vasomotor symptoms, prevent genital
atrophy, prevent migraine headache,
maintain bone density, and show a
favorable lipid profile (small decrease
of LDL and an increase in HDL
concentration).
39. Patients with low risk of
osteoporosis and with atrophic
vaginitis and/or urinary tract
symptoms topical vaginal
estrogen (absorbed systemically
should be given cyclically.
In all condition follow-up these
patients for development of
cancer breast or cancer uterus.
40. C-Other uses of estrogen:
To suppress ovulation in patients
with severe dysmenorrheal.
Hirsutism and amenorrhea due to
excessive secretion of androgens
by the ovary.
To stop excessive uterine
bleeding due to endometrial
hyperplasia.
41. Adverse effects of estrogens:
Post-menopausal bleeding. It is
minimized by treating the patients
with smallest amount of estrogen.
Nausea and breast tenderness. It
is minimized by the use of the
smallest effective dose of
estrogen.
Hyperpigmentation.
42. Migraine headache.
Cholestasis, hypertension, and
gallbladder disease.
With prolonged therapy cancer,
especially breast cancer. Concomitant
administration with progestin
minimizes this risk.
Adenocarcinoma of the vagina in
young women whose mothers were
treated with large doses of
diethylstilbestrol early in their
pregnancy (should be avoided).
43. Contraindications:
In patients with estrogen-
dependent neoplasms e.g.
carcinoma of the endometrium.
In patients with high risk of breast
cancer.
In undiagnosed genital bleeding.
In liver diseases.
In patients with history of
thromboembolic disorder.
45. The Progestins:
Natural Progestins: Progesterone:
I.M.
Progesterone is a precursor of the
estrogens, androgens, and
adrenocortical steroids.
46. Sources:
Ovary ( corpus luteum).
Testis (1.5 mg of progesterone
is secreted daily in male).
Adrenal medulla (synthesized
from cholesterol).
Placenta (during pregnancy).
47. Synthetic progestns:
First and second generations:
Hydroxyprogesterone. I.M.
Medroxyprogesterone. I.M.
Megesterol. Orally
Dimethisterone. Orally
49. Pharmacokinetics:
Progesterone is rapidly absorbed
Short half life (5 min.) small
amounts are store in fat rapidly
and completely metabolized in the
liver (not effective orally)
Metabolism: progesterone
pregnanediol conjugated to
pregnanediol glucuronide
50. Physiologic effects:
Mechanism of action:
Like other steroids: inside the
cell it binds to cytoplasmic
progesterone receptors
binding to response element
hemo- or heterdimers binding
to DNA gene transcription.
51. Effects of progesterone:
Metabolic effects:
Stimulates lipoprotein lipase
Favors fat deposition.
Increases basal insulin levels.
Increases insulin response to glucose
Promotes glycogen storage.
Promotes ketogenesis.
Can compete with aldosterone at the
renal tubules decreases in sodium
reabsorption increases secretion of
aldosterone by the adrenal cortex.
Decreases of plasma level of many
amino acids increases urinary
nitrogen excretion.
52. Increases body temperature.
Alters the function of respiratory
center the ventilatory response
to CO2 is increased reduction in
arterial and alveolar PCO2 during
pregnancy and luteal phase of the
menstrual cycle.
Depressant and hypnotic effects on
the brain.
Alveolar development of the
secretory apparatus of the breast.
Causes maturation and secretory
changes in the endometrium
following ovulation.
53. Synthetic progestins:
First and second generations:
antagonize aldosterone-induced
sodium retention and have slight
androgenic or estrogenic effects.
Third generation: produce a
decidual change in the
endometrial stroma. More
effective gonadotropin inhibitors,
may have minimal estrogenic and
androgenic or anabolic activity.
55. Useful to produce long-term ovarian
suppression (medroxyprogesterone
acetate, 150 mg I.M. ever 90 days)
prolonged amenorrhea, treatment of
dysmenorrhea, endometriosis,
hirsutism, and uterine bleeding
disorders (if estrogens are
contraindicated), and for contraception
(not used for patients planning a
pregnancy in the near future).
To arrest accelerated maturation in
children with precocious puberty.
To treat premenstrual syndrome but in
sufficient doses.
56. Diagnostic Uses:
As a test of estrogen secretion:
administration of 150 mg/d
progesterone, or 10 mg/d
medroxyprogesterone for 5-7 days
followed by withdrawal bleeding in
amenorrheic patients only when the
endometrium has been stimulated by
estrogens.
Test the responsiveness of the
endometrium in patients with
amenorrhea (combined with estrogen).
57. Other ovarian Hormones:
Androgens (testosterone,
androstenedione, and
dehydroepiandrosterone): secreted in
small amounts.
Inhibin inhibits FSH secretion.
Activin increases FSH secretion.
Relaxin increases glycogen
synthesis and water uptake by the
myometrium and decreases uterine
contractility. It facilitates uterine
cervical dilatation and shortens labor.
Follistatin.
Prostaglandins
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