• To define:
–Hirsutism & Virilization
To learn
Physiology of hair growth.
Androgen production in women.
Evaluation of hirsutism.
– osynthesis
– Androgen Types
To Diagnosis, management & treat
hirsutism & Virilization
Objectives
3.
Definition:
• Hirisutism is(not a diagnosis in itself) excess
terminal hair in a male pattern of distribution in
female body as a result of excess androgen and
increase skin sensitivity to androgens.
virilization:
• Frontal bolding
• Deepening of voice
• Musulinization
• clitoromegaly.
4.
• villus hair
issoft, downy, and fine
• Terminal hair
is darker, coarser, and kinkier
5.
• Physiology ofhair growth:
During adolescence, androgens converts vellus
hairs into coarse pigmented terminal hair in
androgen dependent areas.
Different body regions respond differently to
androgens, the reason is unknown. May be:
Number of receptors.
Genetic factors as evidenced by racial hair growth
7.
• Androgen production:
•Adrenal glands
• Ovaries
• Adipose tissue:
(extraglandular production of
testosterone from androstenedione).
• 1. Dehydroepiandrosterone
(DHEA)
• 2. Androstenedione
8.
(DHEA)
• a weakandrogen secreted principally by the
adrenal glands
generally measured as
dehydroepiandrosterone sulfate (DHEA-S)
because of its longer half- life, a more reliable
measure.
9.
• Androstendione:
• aweak androgen secreted in equal
amounts by the adrenal glands and
ovaries
• dihydrotestosterone (DHT)
•an androgen more potent than testosterone
• This metabolic conversion is the result of the
local action of 5α-reductase on testosterone
• within hair follicles and genital skin
• This is the basis for constitutional hirsutism
12.
• dihydrotestosterone (DHT)
•an androgen more potent than testosterone
• This metabolic conversion is the result of the
local action of 5α-reductase on testosterone
• within hair follicles and genital skin
• This is the basis for constitutional hirsutism
13.
• Ovarian androgenproduction is regulated by
luteinizing hormone (LH)
• In conditions of sustained or increased LH
secretion, androstenedione and testosterone
increase.
14.
• When androstenedioneproduction
increases, there is a dependent increase in
extraglandular testosterone production
• In obese women:
• conversion of androstenedione to
testosterone is increased.
• increase in estrone
15.
• Testosterone isthe primary androgen that
causes increased hair growth,acne, and
virilization.
• bound to a carrier protein—sex hormone
binding globulin (SHBG)
• Bound testosterone is unable to attach to
testosterone receptors and is metabolically
inactive
• Only a small fraction(1%–3%) of testosterone is
unbound (free)
16.
• Testosterone receptors
arescattered throughout the body
• Hair follicles
• Sebaceous glands
• Genital skin
Some individuals have increased 5α-reductase
within hair follicles, resulting in excessive local
production of DHT.
• Evaluation:
• History:
•Age onset of hirstusim
• Mensturel history.
• Other evidence of hyperandrognism.
• Drug history: some progestins
POLYCYSTIC OVARY SYNDROME
19.
• Oligomenorrhea oramenorrhea
• Acne,hirsutism
• Infertility
• The disorder is characterized by
• Chronic anovulation
• Excess androgen
Symptoms of PCOS:
20.
Definition of PCOS:Rotterdam cr.
– Physical examination:
– Assess the extent and severity virilization
– Acanthosis nigricanths.
– Laboratory :
– FSH.
– LH.
– Testesteron, estrone.
– Laboratiry investigation for cushing syndrome
– Laboratory investigation of CAH.(17-OH progesterone, plasma
desoxycorticosterone
– Imaging for PCOS
21.
Assessment of PCOS:
–Physicalexamination:
–Assess the extent and severity virilization
–Acanthosis nigricanths.
–Laboratory :
–FSH.
–LH.
–Testesteron, estrone.
–Laboratiry investigation for cushing syndrome
–Laboratory investigation of CAH.(17-OH progesterone,
plasma desoxycorticosterone
–Imaging for PCOS