Hirsutism
Dr. Maha Tarafawy Mohamed
• 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
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.
• villus hair
is soft, downy, and fine
• Terminal hair
is darker, coarser, and kinkier
• Physiology of hair 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
• Androgen production:
• Adrenal glands
• Ovaries
• Adipose tissue:
(extraglandular production of
testosterone from androstenedione).
• 1. Dehydroepiandrosterone
(DHEA)
• 2. Androstenedione
(DHEA)
• a weak androgen secreted principally by the
adrenal glands
generally measured as
dehydroepiandrosterone sulfate (DHEA-S)
because of its longer half- life, a more reliable
measure.
• Androstendione:
• a weak androgen secreted in equal
amounts by the adrenal glands and
ovaries
Testosterone:
A potent androgen secreted by:
•Adrenal glands
•Ovaries
•Adipose tissue from the conversion of
androstenedione
• 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
• 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
• Ovarian androgen production is regulated by
luteinizing hormone (LH)
• In conditions of sustained or increased LH
secretion, androstenedione and testosterone
increase.
• When androstenedione production
increases, there is a dependent increase in
extraglandular testosterone production
• In obese women:
• conversion of androstenedione to
testosterone is increased.
• increase in estrone
• Testosterone is the 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)
• Testosterone receptors
are scattered 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.
Excess androgen production causes:
• Ovarian:
• PCOS.
• Androgen secreating tuomers.
• Adrenal:
• CAH. (21-Hydroxylase Deficiency,11β-Hydroxylase Deficiency).
• Cushing syndrome.
• Testosterone-secreting tumors.
• Other glands:
• Acromegaly
• Sever insulin resistance.
• Idiopathic
• Evaluation:
• History:
• Age onset of hirstusim
• Mensturel history.
• Other evidence of hyperandrognism.
• Drug history: some progestins
POLYCYSTIC OVARY SYNDROME
• Oligomenorrhea or amenorrhea
• Acne,hirsutism
• Infertility
• The disorder is characterized by
• Chronic anovulation
• Excess androgen
Symptoms of PCOS:
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
Assessment of PCOS:
–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
Hirsutism mini presentation Gynecology .ppt
Hirsutism mini presentation Gynecology .ppt

Hirsutism mini presentation Gynecology .ppt

  • 1.
  • 2.
    • 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
  • 10.
    Testosterone: A potent androgensecreted by: •Adrenal glands •Ovaries •Adipose tissue from the conversion of androstenedione
  • 11.
    • 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.
  • 17.
    Excess androgen productioncauses: • Ovarian: • PCOS. • Androgen secreating tuomers. • Adrenal: • CAH. (21-Hydroxylase Deficiency,11β-Hydroxylase Deficiency). • Cushing syndrome. • Testosterone-secreting tumors. • Other glands: • Acromegaly • Sever insulin resistance. • Idiopathic
  • 18.
    • 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