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Reproductive Hormones

Synthesis and Transport Hormones:

The testes and ovaries produce sex


steroids such as androgens and estrogens
from cholesterol.

The ovary converts testosterone to


estradiol, and androstenedione to
estrone.
Peripheral tissues (including those
targeted by androgens) reduce
testosterone to dihydrotestosterone
(DHT), hydroxylate estradiol to estriol,
convert adrenal androgens to
testosterone androgens to estrone and
estriol.
Major transport proteins:
sex hormone-binding globulin (SHBG)
corticosteroid-binding globulin (CBG)
and albumin.
About 1% to 2% of the sex steroids are
free (unbound), the remaining are bound
to proteins (albumin, SHBG and CHG)

Only the free fraction of the hormone is


biologically active.
is the principle androgen hormone in
the blood
is synthesized by the Leydig cells of
the testis of the male; also derived
from progesterone.
is controlled primarily by FSH and LH.
Functions: growth and development
of the reproductive system, prostate
and external genitalia.
Levels demonstrate a circadian pattern
and peak at the time of awakening (8
AM); fall to their lowest level at 8 PM.
There is a gradual reduction in
testosterone after age 30, with an
average decline of about 110 ng/dL every
decade.
Tests for male Infertility: semen analysis;
testosterone, FSH and LH
Reference values: 3.9-7.9 ng/mL (serum)
1. Testosterone

Transport Proteins:
Sex hormone binding-globulin (SHBG) 60%
Albumin 40%

the concentration of binding protein


determines the level of total testosterone but
not the free testosterone levels during
laboratory estimation.
is the principal androgen formed by
adrenal cortex; weak androgen.
this androgen is primarily derived from
the adrenal gland.
it is valuable in the assessment of
adrenal cortical function.
Negative
feedback for
FSH and LH.
Clinical disorders
Types of testicular infertility
a. Pretesticular infertility
a. Due to hypothalamic or pituitary lesion
b. Testosterone, FSH, LH normal or decreased

b. Testicular infertility
Congenital (cryptorchidism, Klinefelters syndrome, 5-
alpha reductase deficiency) acquired (varicocele,
tumor, orchitis)
Testosterone (decrease), FSH and LH (increase)
c. Post testicular infertility
Due to disorders of sperm transport and
function
Testosterone, FSH, LH normal
Disorders of sexual development and Testicular
Hypofunction
Hypergonadotropic hypogonadism
Klinefelters syndrome (low testosterone, high
FSH and LH)
Testicular feminization syndrome
Myotonic dystrophy, gynecomastia
Testicular injury and infection
Extra X chromosome
Hypergonadotropic hypogonadism
Klinefelter
syndrome or Klinefelter'
s syndrome,
also 47,XXY or XXY
syndrome
Due to an extra
chromosome
Characterized by small
firm testicles,
gynecomastia and
azoospermia
Hypergonadotropic hypogonadism
Testicular feminization syndrome
A.k.a: Androgen insensitivity syndrome
Lack of androgen
Characterized by developed female physical
attributes
Complete
Female external genitalia, no uterus
Raised as female with female identity
Partial
Can have genital that looks female/ both female
and male
Can be raise either as male / female
Hypergonadotropic hypogonadism
Myotonic
Dystrophy
Most common form of
muscular dystrophy that
begins in adulthood.
Characterized by:
Hypogonadism. Muscle
weakness, frontal
balding, DM, muscle
dystonia
Hypergonadotropic hypogonadism

SERTOLI CELLONLY
SYNDROME
Aka: Germ cell aplasia
cause of male infertility
Hypergonadotropic hypogonadism

NOONAN SYNDROME
Characterized by mildly unusual facial
features, short stature, heart defects,
bleeding problems, skeletal malformations.
referred to as the male version of Turner's
syndrome
Hypergonadotropic hypogonadism

TESTICULAR INJURY and INFECTION


Viral orchitis
HIV infection
Radiation &chemotherapy
Hypergonadotropic hypogonadism

5 REDUCTASE DEFICIENCY
Condition that affects male sexual development
before birth & during puberty
Characterized with decreased levels of the
enzyme and development of female characteristics
Hypogonadotropic Hypogonadism

1.) Kallmanns syndrome (low testosterone, low FSH


and LH)

2.) Hyperprolactinemia
Drug induced or prolactin-producing tumors of the
pituitary

3.) Pituitary disease


Due to surgical trauma, tumors
is carbon-18 steroid hormones that have a
phenol A ring.
it arises through structural alteration of the
testosterone molecule.
it is not produced by the ovaries after
menopause.
Functions: promotion of breast
development, maturation of the external
genitalia, deposition of body fat and
termination of linear growth (secondary
sexual characteristic in the female)
In conjunction with progesterone, they
function in uterine growth and regulation of
menstrual cycle, and maintenance of
pregnancy.
Deficiency: irregular and incomplete
development of the endometrium.
Precursor: acetate, cholesterol,
progesterone and testosterone
3 forms: estrone, estradiol and estriol
Estrone and estriol are metabolites of
intraovarian and extraglandular conversion.
3. Estrogen
a. Estrone (1 ) is the most abundant
estrogen in post menopausal women.
b. Estradiol (2 ) is the most potent
estrogen secreted by the ovary; major
estrogen. Is the most abundant in pre
menopausal women; low levels in the
menopausal stage. It is synthesized
from the testosterone, then diffuses
out of the thecal cells of the ovaries in
the female
3. Estrogen
it is the precursor of both 1 and 3 ;
it is used to assess ovarian function;
serves as negative feedback for FSH.
transport proteins: albumin (60%) and
SHBG (38%)
the free form of 2 is approximately 2%.
3. Estrogen
c. Estriol (3 ) is a metabolite of estradiol. Is
the estrogen found in maternal urine. Is
the major estrogen secreted by the
placenta during pregnancy formation in
a pregnant women is dependent on fetal
and placenta function. It is used to assess
the fetoplacental unit (fetoplacental
viability), postdate gestations and
intrauterineretardation.
3. Estrogen
it promotes uteroplacental blood flow
as potently as other estrogens.
it is used as a marker for Down
syndrome (together with AFP and HCG)
preferred specimen: plasma
is a carbon-21 compound in the steroid
family.
it is produced mainly by the granulose
(lutein) cells of the corpus luteum in the
female.
is the prime secretory product of the
ovary.
it is a dominant hormone responsible
for the luteal phase cycle among
females.
it serves to prepare the uterus for
pregnancy and the lobules of the breast
for lactation.
it is intermediate in the synthesis of
adrenal steroids and androstenedione.
Deficiency: failure of implantation of
embryo.
Metabolites: pregnanediols (most
easily measured metabolite),
pregnanediones, pregnanalones
Test for menstrual cycle dysfunction
and anovulation: estrogen,
progesterone, FSH, LH
Test for female infertility: HCG, PRL,
FT, TSH, FSH, LH, estradiol and
progesterone
- FSH & LH regulate
control of estrogen
and progesterone.

- Estrogen and
progesterone
control the FSH &
LH.
Relaxin
In the female, it is produced by the COPUS
LUTEUM of the OVARY , the breast , and
During pregnancy also by
the PLACENTA, chorion, and decidual
In the male, it is produced in the prostate and is
present in human semen.
Activin
enhances FSH secretion and induces
steroidogenesis

Inhibin
Produced in ovaries inhibits FSH production
Hormonal control of ovulation
Central control of FSH & LH secretion from the
anterior pituitary resides in GnRH from hypothalamus
Positive & negative feedback responses exist among
estrogen, progesterone, LH & FSH production
A midcycle surge in LH production stimulates a series
of events that culminates in ovulation, with FSH levels
falling thereafter
You would perform an LH level in this phase to
determine if ovulation is happening
Increase Luteinizing hormone will trigger:
Release of estrogen
Formation and growth of ovarian follicle
Release of eggs from the ovaries
Decrease progesterone & estrogen
Ovulation
Formation and growth ovarian follicle
Release of eggs from the ovaries
Menstrual Cycle abnormalities
Amenorrhea
Oligomenorrhea
irregular menstrual bleeding
Cycle lengths excess of 35-40 days
Menorrhagia
Uterine bleeding in excess of 7 days
Hypogonadotropic hypogonadism
Deciciency of FSH & LH, can cause secondary amenorrhea
Hypergonadotropic hypogonadism
Ovarian failure with elevation of FSH concentration
Type 1: Hypothalamic hypogonadism
Hypothalamic amenorrhea (anorexia nervosa,
idiopathic, exercise induced)
Kallmanns syndrome
Isolated gonadotropin deficiency

Type 2: Estrogenic chronic anovulation


Hyperthecosis

Type 3: Hyperthalamic hypogonadism


Premature ovarian failure
Turners syndrome
Placenta
Human placental lactogen
placental glycoprotein hormone with physiologic
effects similar to LH
Produced by placenta & measured in urine, serum,
amniotic fluid
It stimulates development of mammary gland
Important in diagnoses of intrauterine growth
retardation
Potent lactogenic properties.
Secretes estrogen, progesterone & b-HCG
Human chorionic gonadotropin
Produced by trophoblast cells of placenta during
pregnancy
It serves to maintain progesterone production by the
corpus luteum in the early pregnancy
HCG beta subunit (similar to LH) marker for
pregnancy
Increase in 1st trimester, decrease in 2nd & 3rd
Tumor marker for testicular carcinoma in males