undergraduate course lectures in Obstetrics&Gynecology prepared by DR Manal Behery Professor of OB &Gyne Faculty of medicine ,Zagazig University

1. Dr Manal Behery
Prof OB&GYNE ZAGAZIG UNIV
2014

2. Source of androgens in women
•
1-Ovarian theca and stromal cells <LH control
2-Adrenal cortex
3- Peripheral (< pre cursors)
 Skin
 Adipose tissue
 Liver
 Placenta

3. Function of androgen in women ?
 Estradiol production (aromatisation in
granulosa cells <FSH control)
 Sex drive
 Muscular mass, etc…

6. The production rate of
testosterone in the
normal female is
0.2 to 0.3 mg/day
Normal total testosterone
concentration in serum
is below 0.8ng/ml
6

7. Androgen in circulation
7
Normal women Hirsute women
80% SHBG 79% SHBG
19% Albumin
19% Albumin
1% Free 2% Free

8. Types of hair
Lanugo
Fetal hair
Vellus
Short,
fine,
Unpigmented
Before puberty
Terminal
Long, coarse,
pigmented
arises from vellus
hair

9. Androgen increase in the transformation of the vellus to terminal hair
& increase sebaceous Follicle activity

10. Hirsutism:
Excessive growth of terminal hair in male
sexual sites.

11. Hypertrichosis
Excessive growth of thin vellus hair at any
body site
Drug-induced hypertrichosis

12. Causes

13. .
Hirsutism is a consequence of several factors
1.Androgen production
2. The sensitivity of the androgen receptors at
the level of the hair follicle.
3.The activity of 5œ-reductase

14. Role of 5-Reductase
 Converts
Testosterone to
Dihydrotestostero
ne in hair follicles
 Is increased in
both idiopathic
and other forms
of hirsutism

15. •the commonest cause (90%).
•
•More in African, Mediterranian population.
•Positive family history.
•* No menstrual abnormalities.
* due to increased sensitivity of hair follicle
1) Constitutional (idiopathic):

16. (2) Ovarian cause:
1. PCO “→ the commonest cause.
2. . Stromal hyperthecosis.
3-Pregnancy luteoma
3. Androgen secreting tumors:
- Sertoli-lyedig tumors.- Gynandroblastoma.

17. Ovarian causes

18. Reproductive cycle regulated by HPO axis

19. LH, FSH
androgen
Estrogen
GnRH
Anovulation
H-P-O axis Dysfunction in PCOS

21. (3) Adrenal cause:
1.Congenital adrenal hyperplasia.
2. Cushing syndrome.
3. Androgen secreting tumors.
Congenital adrenal hyperplasia

22. 4) Pituitary cause:
* Pituitary adenoma
"Prolactinoma".
 * Growth H. secreting
tumor.acromegaly

23. Anabolic steroids
Danazol
Metoclopramide
Methyldopa
Phenothiazines
Progestins
Reserpine
Testosterone
5) Iatrogenic:

24. (6) Obesity

25. hirsute alone
hirsute with pilosebaceous unit
overactivity (acne)
hirsutism and ovulatory disorders
hirsutism and signs of virilization
Presentation of hirsutism

26. The clinical evaluation of hirsutism
 When and where is the hair?
 Weight and menstrual history
 Family history
 Drugs
 Acne
 Symptoms or signs of virilisation
• Temporal hair loss
• Voice change
• Clitoral enlargement

28. Ferriman-Gallwey hirsutism scoring system

30. CLASSIFICATION

31.  Hirsutism:Ferriman-
Gallwey Scoring
System
Acne: 50%
Mild
 moderate
severe

32. General examination
.
Thyroid disease,
Cushing syndrome,
Signs of virilization,
Signs of insulin resistance
e.g. acanthosis nigricans.

33. Acanthosis Nigricans
• Velvety plaques on nape of
neck and intertriginous areas
• Associated with insulin
resistance

35. .Breast:
Galactorrhea
{Hyperprolactinaemia can be accompanied by
increase in adrenal androgen}
Breast atropy

36. Pelvic exam for ovarian mass

37. Investigations
 Investigations are needed if:
 Hirsutism occurs in childhood
 There are features of virilization

 Hirsutism is of sudden or recent onset
 There is menstrual irregularity or cessation

38. Testosterone ng dl)
>200 <200
U/S of the ovary Anovulation
(PRL, TSH)
Adenxal mass Nothing
Laparotomy CT of the adrenala & ovaries
Laparotomy

39. Total Testosterone (T)
DHEA-S (DS)
17-hyroxyprogesterone (17-OHP)
T > 200 ng/dl
DS > 700 μg/dl
Suspect Tumor
17-OHP > 2 ng/ml
Suspect CAH
T Elevated
±
DS Elevated
DS Elevated
T & DS Normal
PCOS
Adrenal
Idiopathic
Laboratory Evaluation

40. PCOS T
LH/FSH
usually inc
2/1
Late-onset CAH 17-OH-P >200 ng/dL
Androgen-secreting ov tumor Total T >200 ng/dL
Androgen-secreting ad tumor DHEAS >700 g/dL
Cushing syndrome Cortisol Increased
Exogenous androgen use Toxicology
screen
Increased

41. TREATMENT

43. OCPs: first option when fertility is not desired
 Decrease in LH secretion and decrease in
androgen production
 Increase in hepatic production of (SHBG)
 Decreased adrenal androgen secretion

44. Cyproterone acetate:
A progestin with strong antiandrogenic action.
Inhibits gonadotrophin secretion and compet
efor androgen receptors on target organs
Dosage-
100mg from D5-D14 with ethinyloestradiol
30µg, from D 5 to D25

45.  Androgen receptors blockade
 Suppression of Androgen biosynthesis
 Increased metabolic clearance of teststerone
( Testosterone  Estrogen )
 50-200 mg/day pd
 Spironolactone + OC is well established regimen
Spironolactone, 50-200 mg per day

46. Insulin-Sensitizing Agents
 Induction of ovulation
 Some reduced hair growth
 Improved glucose utilization
 Lowered serum insulin
 Lipid lowering properties

47. 47
FLUTAMIDE :
 Blocks the androgen receptors
 Decreases androgen production
 Usually used with Ocs
KETOCONAZOLE:
 Equally effective but danger of liver
toxicity
 Last resort of treatment.

48. Electrolysis:
.
Needle is inserted into the hair follicle
•a current is used to destroy the dermal papilla.
•All areas, usually the face
•May give permanent removal
•Pain, scarring, painful, repeat treatments needed, time consuming,
expensive, pigmentation

49. b. Laser & intense pulsed light
• A light source sufficient to penetrate to the follicular bulge & the papillae is
directed at the hair by probe.
•All areas
•May give permanent hair reduction, efficient, painless
•Dark hair required, expensive, scarring, skin pigmentation, repeated treatments
usually necessary

50. Treatment options for hirsutism
 Counselling
 Cosmesis
 Combined Oral Contraceptive
 Cyproterone acetate
• With or without COC e.g. Diane
 Spironolactone
• Causes irregular periods
 Topical Eflornithine

51. Questions?