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TINNY RASJAD INDRA SpPK (K)

Hormones synthesized by :
Testis testosterone
Ovary progesterone and estradiol
Pituitary follicle stimulating hormone (FSH)
luteinizing hormone (LH)
Hypothalamus gonadottropin releasing hormone
(GnRH)
Placenta human chorionic gonadotropin
(hCG)
estrogens
progesterone
 Regulation of
reproduction
in male

LH Luteinizing hormone
FSH Follicle-stimulating
hormone
GnRH Gonadotropin
-releasing hormone
 Hypothalamus secretes GnRH binds to specific cell
membrane receptor on gonadotroph in the anterior
pituitary synthetize and secrete LH and FSH
FSH induces Sertoli cells to synthetize and secrete
androgen-binding protein maintains high testosterone
concentration.
LH induces Leydig cells to synthesize and secrete
testosterone
Testosterone is required for normal spermatogenesis and
normal male growth, some transported to hypothalamus
and anterior pituitary where it has a negative feedback
effect.
Regulation of
reproduction
in female
 Hypothalamus secretes GnRH binds to specific
cell membrane receptor on gonadotroph in the
anterior pituitary synthesize and secrete LH and
FSH
Regulatory process in female is cyclic menstrual
cycle pituitary, ovarian and uterine changes
occur during 28 days
FSH regulating follicular phase of the ovarian cycle
Growing follicle produces estradiol restores
endometrium proliferative phase
 Estradiol has a negative-feed back on hypothalamus
and anterior pituitary
Near the end of the follicular phase, feed back
effect of estradiol switches to positive surge in
GnRH, FSH and LH secretion ovulation
Estradiol production drops
Disrupted follicle differentiate into corpus luteum
(luteal phase of the ovarian cycle) synthesize
and secrete estradiol and progesterone cause
development of endometrium (secretory phase of
endometrium)
Infertile cycle :
Corpus luteum regress estradiol and
progesterone synthesis and secretion decrease
endometrium shed during menstruation
Hypothalamic and anterior pituitary negative feed
back decrease FSH and LH are synthesized and
secreted again to begin another cycle
 9 days after fertilization implantation trophoblasts
synthesize hCG (human chorio gonadotropin, a LH like
hormone) are found in maternal blood
hCG prevents corpus luteum from regression estradiol
and progesterone synthesis continues maintain
uterine endometrium throughout pregnancy
 Benign Prostatic Hypertrophy
Prostate Cancer
Infertility
Male
Female
Endometriosis
Pelvic Inflammatory Disease
Ovarian Cysts
Cancer : breast, cervix, uterine
 Common in older men; varies from mild to
severe
Change is actually hyperplasia of prostate
Nodules form around urethra
Result of imbalance between estrogen and testosterone
No connection w/ prostate cancer
Rectal exams reveals enlarged gland
Incomplete emptying of bladder leads to
infections
Continued obstruction leads to distended
bladder, dilated ureters, renal damage
If significant, surgery required
Lab test : PSA (Prostat Specific antigen) normal/
increase 4 10 ng/ml (in 20% patients)
 Cause not determined
Genetic, environmental, hormonal factors
Common in North American and northern
Europe
Incidence higher in black population than
white
Genetic factor?
Testosterone receptors found on cancer cells
 Hard nodule in periphery of gland
Detected by rectal exam
No early urethral obstruction
b/c of location
As tumor develops, some obstruction occurs
Hesitancy, decreased stream, urinary frequency,
bladder infection
 2 helpful serum markers
Prostate-specfic Antigen (PSA) > 10-40 ng/ml
Useful screening tool for early detection
Prostatic acid phosphatase (PAP)
elevated when metastatic cancer present
Ultrasound and biopsy confirms
 Surgery and radiation
Risk of impotence or incontinence
When tumor androgen sensitive:
orchiectomy (removal of testes) or
Antitestosterone drug therapy
5 yr survival rate is 85-90%
 The main reproduction problem a couple visits their
physician is INFERTILITY

Definition : inability to conceive after 12

months of unprotected sexual intercourse.
 Plays a role in 1/3 of infertile couples.
Causes of male infertility :
Primary hypogonadism (30 40%)
Disorders of sperm transport (10 20%)
Secondary hypogonadism (2%)
Unknown etiology (50%)
Isolated impaired spermatogenesis :
Y chromosome microdeletions and substitutions
Viral orchitis,Tuberculosis,STDs
Radiation,Chemotherapeutic agent
Environmental toxins
Prolonged elevation of testicular temperature
 Can be solely male, solely female, or both
Considered infertile after one year of
unprotected intercourse fails to produce a
pregnancy
Male problems include
Changes is sperm or semen
Hormonal abnormalities
Pituitary disorders or testicular problems
Physical obstruction of sperm passageways
Congenital or scar tissue from injury
Semen analysis
Assess specific characteristics
Number, motility, normality
Clinical features :
Evidence of hypogonadism may be present
Testicular size and consistency may be abnormal,
varicocele may be apparent on palpation
Key diagnostic test : semen analysis sperm
counts <13 million/mL, motility : <32%, and <9%
normal morphology subfertility.
If the sperm count is low on repeated exam , or if
there is clinical evidence of hypogonadism,
hormone level should be measured.
 NORMAL VALUE IN SEMEN ANALYSIS

VOLUME 2 5 mL
VISCOSITY Pours in droplets
pH 7.2 8.0
SEMEN > 20 million/mL
CONCENTRATION
SPERM COUNT > 40 million/ejaculate
MOTILITY > 50% in 1 hour
QUALITY > 2 or a, b, c, according to sperm motility
grading
MORPHOLOGY 14% normal forms (strict criteria)
>30% normal forms (routine criteria)
ROUND CELLS < 1 million/mL
 Sexual abstinence 3 4 days before specimen
collection
When performing fertility testing, 2 3 test
performed with 2 weeks intervals
Provide warm sterile glass or plastic container
Inform the patient not to void into the container
Avoid collecting semen in condom spermaticide
Semen collected at home should be send
immediately in room temperature within 1 hr
Record the time specimen collected and receipt
Examination :
Appearance greyish white, translucent, with
specific odor
Liquefaction a fresh specimen liquify
within 30 60 min after collection. Failure to
liquify indicates deficient in prostatic
enzyme
Volume : 2 5 mL decreased volume
associated with infertility
Viscosity : refers to the consintency of the
fluid increased viscosity and incomplete
liquefaction will impede sperm motility
 pH : alkaline, 7.2 8.0.
Increased pH indicative of infection.
Decreased pH increased production of prostatic fluid
Sperm count
Normal count >20 million/mL or >40 million/ ejaculate
(only developed sperm should be counted)
!0 20 million/mL considered borderline
Round cells : undeveloped sperm / WBC
> 1 million/mL leukocytes indicates infection of
reproductive organ that leads to infertility perform
aerobic and anaerobic culture
 Spermatides >1 million/mL indicates
spermatogenesis disruption usually caused
by viral infection, exposure to toxic
chemicals, and genetic disorders
Sperm motility
Capability of sperm cells to move forward is
criticial for fertility. Motility is evaluated by
both speed and direction. A minimum
motility of 50% with 20% rating after 1hour is
considered normal
 SPERM MOTILITY GRADING

GRADE WHO CRITERIA

4.0 a Rapid, straight motility
3.0 b Slower speed, some lateral
movements
2.0 c Slow forward progression,
noticeable lateral movement

1.0 d No forward progression

0 e No movement
 Sperm morphology
Evaluation of head, neck piece, mid piece
and tail and their size, acrosomal cap and
vacuolization
The head represents the sperm cell itself
with its enzyme-containing acrosomal cap
Find abnormal heads : double head, giant
head, pin head, tapered head and
constricted head
Abnormal tail : coiled, bend, doubled
Long neck piece backward bending head
 ADDITIONAL TEST FOR ABNORMAL SPERM ANALYSIS
Abnormal Result Possible Abnormality Test
Decreased motility Viability Eosin-nigrosin stain
with normal count
Decreased count Lack of seminal vesicle Fructose level
support medium
Decreased motility Male antisperm Mixed agglutination
with clumping antibodies reaction
Immunobead tests
(Sperm agglutination
with male serum)
Normal analysis with Female antisperm Sperm agglutination
continued infertility antibodies with female
serum/cervical mucosa
Etiology :
Primary hypogonadism testicular failure

Secondary hypogonadism hypothalamic-

pituitary defects
Diagnose :
Testosterone level
Gonadotropin levels (LH and FSH) are

Etiology :
Klinefelters syndrome most common
Acquired primary testicular failure results from viral
orchitis, trauma, cryptorchidism, radiation damage,
systemic diseases (amyloidosis, Hodgkins disease, sickle
cell disease).
Toxins marijuana, alcohol, heroin, lead,
antineoplastic, and chemotheurapeutic agents.
Ketoconazole blocked testosterone synthetis.
Competitive inhibition by spironolactone and
cimetidine.
Diagnose :
Testosterone levels low
Gonadotropin levels low (hypogonadotropic
hypogonadism)

Etiology :
Kallmanns syndrome : impairment of
synthesis/release GnRH (gonadotropin releasing
hormone) LH, FSH with/without anosmia
Cushings syndrome, adrenal hypoplasia- congenita,
hemochromatosis, hyperprolactinemia
 History focus on developmental stages such as
puberty and growth
Physical examination should focus on secondary sex
characteristics : hair growth in the face, axilla,
chest, pubic region, gynaecomastia, testicular
volume, prostate, height and body proportion.
The presence of varicocele
Morning total testosterone levels <6.93 nmol/L
(<200 ng/dL), in association with symptoms,
suggests testosterone deficiency.
 Levels between 6.93 nmol/L and 12.13
nmol/L must be repeated and a free
testosterone levels should be measured.
Levels of LH and FSH can be used to
differentiate between primary and secondary
hypogonadism.
Measurement of prolactin level and MRI scan
of the hypothalamic-pituitary region should
be considered in secondary hypogonadism
 FSH
OESTROGENE OESTRIO
GRAAFIAN
S L
LH FOLLICLES
OVULATION PROGESTERON
OESTROGENES
CORPUS
LUTEUM

PITUITARY Gn-RH UTERUS

HYPOTHALAMUS hCG
 LH FSH Oestradiol- Progesteron
(u/L) (u/L) 17 (nmol/L)
(pmol/L)
Children 13 13 40 120 <6
Menstruating adults
Follicular phase 1 - 10 16 40 600 <6
Mid-cycle peak 8 60 4 15 500 1600 4 10
Luteal phase 2 14 15 280 1000 > 20
Post menopause > 15 > 20 < 150 <6
 The pituitary hormone : luteinizing
hormone (LH), follicle stimulating
hormone (FSH), stimulate ovarian
follicular development and result in
ovulation at about day 14 of the 28-
day menstrual cycle.
 Associated w/ hormonal imbalances
Result from altered function of hypothalamus, anterior
pituitary, or ovaries
Typically after long use of birth control pill
Structural abnormalities
Small or bicornuate uterus
Obstruction of fallopian tubes
Scar tissue or endometriosis
Access of viable sperm
Change in vaginal pH
Due to infection or douches
Excessively thick cervical mucus
Development of antibodies in female to particular sperm
Smoking by male or female
 Broad range of tests avail
General health status checked 1st
Pelvic examinations, ultrasound, CT scans check
for structural abnormalities
Tubal insufflation (gas/pressure measurement) or
hysterosalpingogram (X-ray w/ contrast material)
used to check tubes
Blood tests throughout cycle to check hormone
levels
 Due to primary (gonadal)
secondary (pituitary)
Basal tests
Preliminary investigation :
Plasma / urine [estriol]
Total urinary estrogens
Low value confirm gonadal failure but do not
diferentiate the ovarial / pituitary site
To confirm the site, need to measure plasma
[FSH],
[LH], urinary excretion of [FSH] and [LH],
plasma
prolactin, [oestradiol-17] and progesterone
Gonadal failure due to gonads disease
The ovaries fail to respond to endogenous
gonadotrophin no progesteron nor
oestrogens produced lack of feed back
inhibition to pituitary and hypothalamus
plasma [LH] and [FSH]
Gonadal failure due to non gonadal causes
Primary causes : hypothalamic or pituitary or
both
Plasma [LH] and [FSH] are low or normal-low
while plasma oestradiol-17 and
progesterone are low
In Stein-Leventhal syndrome (polycystic
ovary) primary pathological abnormality
lies in the hypothalamus / pituitary. Plasma
[LH] and [tertosterone] , plasma
[oestrogens]
 Hyperprolactinemia happens in 20% of
women with secondary amenorrhoe and
ovulatory failure.
Some have galactorrhoea
1. Plasma [progesterone] or 24 hr urinary pregnandiol
excretion about the 21st day of menstrual cycle + basal
temperature charts.
2. Plasma or urinary [oestrogens] low value confirms
gonadal failure primary/secondary
3. Plasma [FSH] = probably has primary ovarian
failure. If normal / low proceed to 4)
4. Plasma [prolactin] , confirm that she does not under
stress / consuming oral conraceptives to perform
thyroid function. If normal / low proceed to 5)
5. Dynamic tests. Using GnRH test, if subnormal due
to pituitary failure secondary to hypothalamus
disease.
 Synthetized by placental syncytiotrophoblast
Secreted into maternal circulation and excreted
in maternal urine in very early stage of
pregnancy
Urinary hCG output peaks about 7th 10th weeks
With LH like effect against corpus luteum to
maintain steroids production
hCG produced in other conditions, by
trophoblastic tumors in male / female
Male : testicular teratoma
Female : hydatidiform mole and choriocarcinoma
 Endometriosis is typically seen during the
reproductive years;
occurs in roughly 610% of women.
Symptoms may depend on the site of active
endometriosis. Its main but not universal
symptom is pelvic pain in various
manifestations.
is a common finding in women with
infertility.
 Endometriosis is a gynocological condition in
which cells from the lining of the
Uterus(endometrium) appear and flourish
outside the uterine cavity, most commonly
on the membrane which lines the abdominal
cavity, the peritoneum. The uterine cavity is
lined with endometrial cells, which are under
the influence of female hormone
Signs and symptoms
Pelvic pain
dysmenorrhoe
Chronic pelvic pains
dyspareunia painful sex
dysuria urin
 Endometriosis lesions react to hormonal
stimulation and may "bleed" at the time of
menstruation. The blood accumulates locally,
causes swelling, and triggers inflammatory
responses with the activation of cytokines. This
process may cause pain. Pain can also occur from
adhesions (internal scar tissue) binding internal
organs to each other, causing organ dislocation.
Fallopian tubes, ovaries, the uterus, the bowels,
and the bladder can be bound together in ways
that are painful on a daily basis, not just during
menstrual periods.[
SELAMAT
BELAJAR