2. Each hair follicle develops at about 8-10wks of
gestation as a derivative of epidermis.
Number of hair follicles is set from birth
Main difference between sexes is the degree of
differentiation of the hair
Hair grows in a mosaic pattern(in a given area ,hair
are in different stages of development)
2
3. Adults have two types of hair: Vellus and Terminal.
Vellus hair : Soft, fine, colorless, and usually short.
Grow on the face, chest, and back and
give the impression of "hairless" skin.
Terminal hair : longer, coarser, darker hair that grows
on the scalp, pubic, and armpit areas in
both adult men and women.
4. Anagen : Growth phase,85- 90 % of the life cycle
Catagen : The transitional period from growing to
resting lasting 2 to 4 weeks
Telogen : Quiescent phase ,lasting 2-4 months
The growth phase or the anagen phase is primarily
influenced by disorders that stimulate hair growth
as well as therapeutic modalities.
5. Androgen sensitive hair :
Depend upon androgen input for hair growth.
Face , neck, chest ,abdomen ,axillary, upper arms
,inner thighs and pubic hair, part of the scalp hair.
Less Androgen dependent :
Forearms ,hands , lower legs
9. 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
10. Normal women Hirsute women
80% SHBG 79% SHBG
19% Albumin 19% Albumin
1% Free 2% Free
11. IT MAY BE EITHER
HYPERTRICHOSIS
HIRSUTISM
VIRILIZATION
11
12. HYPERTRICHOSIS : REFERS TO HAIR DENSITY
OR LENGTH BEYOND THE ACCEPTED LIMITS
OF THE NORMAL FOR THE PARTICUALR
AGE,RACE OR SEX.
• May be generalised or localised and may consist of
lanugo, vellus or terminal hair.
• Frequently associated with the use of medication
such as antiepileptics
12
13. HIRSUTISM : APPEARANCE OF EXCESSIVE COARSE
(TERMINAL)HAIR IN A PATTERN NOT NORMAL IN
THE FEMALE
The abnormal distribution of excess hair growth ,such
as face ,chest or upper abdominal hair
Affects 5-10% of women
May also signal the presence
of a hormone imbalance or a
hormone-producing tumor.
13
dpankar
14. VIRILIZATION : REFERS TO CONCURRENT
PRESENTATION OF HIRSUTISM WITH A
BROAD RANGE OF SIGNS SUGGESTIVE OF
ANDROGEN EXCESS,SUCH AS
Acne,
Frontotemporal balding,
Deepening of the voice ,
Decrease in breast size
Clitoral hypertrophy
Increased muscle mass
Amenorrea / oligomenorrhea
14
15. Increased serum androgens
Decreased levels of SHBG-> increased free testosterone
Increased responsiveness of target organ to normal
circulating androgens
Increased activity of 5 alpha reductase
Normal women Hirsute women
80% SHBG 79% SHBG
19% Albumin 19% Albumin
1% Free 2% Free
22. Tumors of the ovaries and the adrenal glands secrete excess
hormones including androgen.
Ovarian tumors Adrenal tumors
Granulosa -theca cell tumors Adrenal adenoma
Arrhenoblastoma Adrenal carcinoma
Gonadoblastomas
Lipoid cell tumors ACTH secreting tumors
Dysgerminoma
Brenner's tumor
23. Functional adrenal hyperandrogenism
Hypereactio luteinalis of pregnancy - transient increase
in androgen levels during pregnancy
Thecoma of pregnancy - Transient androgen secreting
tumor during pregnancy
True hermaphroditism - condition where both male and
female internal sex organs are present
24. Genetics
There are very obvious family and racial differences in
hirsutism patients. In some women, the skin is very
sensitive to even low levels of androgens and their
follicles produce primarily terminal (coarse and dark)
hair.
25. In 70-80 % cases of hirsutism
5-10% of women in reproductive age
Fulfills the Rotterdam criteria
Hyperandrogenism
Amenorrhoea /oligomenorrhoea
USG features of PCOD
Anovulation
Infertility
Obesity
28. It is a familial disorder of adrenal steroid
biosynthesis
Autosomal recessive mode of inheritance.
The defect is expressed as adrenal enzyme
deficiency.
5 major Enzymes deficiencies are clinically
important
21-Hydroxylase
11-b-Hydroxylase
17-a-Hydroxylase
3-b-Hsteroid hydrogenase
20,22 Desmolase deficiency
29. The enzyme deficiency causes
reduction in end-products,
accumulation of hormone precursors
& increased ACTH production.
The clinical picture reflects the
effects of inadequate production of
cortisol & aldosterone and the
increased production of androgens &
steroid metabolites.
31. In less severe forms (late onset CAH)
Genitalia is normal at birth.
Precocious pubic hair &
Clitoromegaly
Excess facial or body hair appear later in
childhood, often accompanied by tall stature
Varying virilizing symptoms ranging from
oligomenorrhea to hirsutism and infertility
35. A very rare disease
The clinical state of increased free circulating
glucocorticoid
36. Hypercotisolism
Lipid mobilization
Lipid Catabolism
Moon-face
buffalo hump
truncal obesity
Violaceous striae
Hepatic glucose
production ↑
Insulin resistance
Glucose intolerance
Hirsutism(65%)
Protein metabolism
Negative nitrogen balance
Disruption of water and
electrocytes metabolism
Proximal muscle
weakness
Dependent edema
Hypertension
Hypokalemic
Metabolic alkalosis
Lipid redistribution
37. History- Onset and progression
Physical examination
Assess the severity of hirsutism (+/- virilisation)
Acertain the underlying cause
Investigations
Treatment
38. Onset and progression
Most of the causes begins in early adolescence
Presentation may be late depending upon the cause
Rapid progression – androgen secreting tumors
39. Degree and extent
Ferriman gallwey scale
Quantifies the extent of hair growth in 9 most
androgenic sensitive sites
Hair growth is graded 0-4 at each site
Score of 8 or more (max 36) indicates hirsutism
40.
41. Associated signs of virilisation
(May occur in CAH, HAIR-AN syndrome, Androgen secreting
tumor, Acanthosis nigricans)
Clitoral hypertrophy
Deepening of voice
Acne
Male pattern baldness
Breast atrophy
Android habitus
42. History of drug intake producing androgenicity
Family history- correlated
Mild hirsutes- during puberty, pregnancy, postmenopause
Hirsutism with rapid onset- Evaluation for adrenal /ovarian
tumor
High testosterone levels (>200ng/100ml)- Androgen
producing tumor
Patients with primary amenorrhoea with virilism-
karyotyping for y carrying dysgenetic gonads
43.
44. Late onset CAH-
D/t partial deficiency of 21- hydroxylase enzyme
17- OHP is elevated
Cushing disease-
24 hr urinary free cortisol excretion- (10-90µg)
Late evening plasma cortisol level – (< 15 µg/dl )
Overnight Dexa suppression test
45. Adrenal tumors
Any age
Rapid onset
Hirsutes++
Virilism+
Amenorrhoea
DHEAS ↑↑(>700µg/100ml)
T- normal or ↑
Dexa suppression test- negative
IVP
CT-scan
MRI
Any age
Rapid onset
Hirsutes++
Virilism+
Amenorrhoea
T- ↑( >200 ng/100ml)
DHEAS- normal
Sonography
Laparoscopy
biopsy
Ovarian tumors
46. Diagnosis Menstrual Total DHAS LH 17OHP Sourse of
Pattern Testoste- Androgens
rone
PCOS Irregular Elevated mildly Elevated Normal OVARY
elevated
CAH Irregular Elevated Often Usually Markedly Adrenals
Normal Normal elevated
Idiopatic Regular Normal Normal Normal Normal Skin
hirsutism
47. Principles of management
To remove excess hair
To suppress or neutralise the action of androgen
To remove the source of excess androgen
48. Best results are achieved by combination treatment
including antiandrogens, suppression and topical
treatments
Goal should be to reduce the time spent mechanically
removing unwanted hair.
The choice of drug depends mainly on its tolerability by
each individual patient.
50. Drugs- ( depending upon the site of production of
excess androgens)
OCPS
Progestrogens
Antiandrogens
Spironolactone
Dexamethasone
GnRH Analogues
Combined approach
52. CLINICAL BENEFITS
Helpful in treatment of Hirsutism
Excellent cycle control
Decreases acne
No weight gain.
METABOLIC BENEFITS
No effect on carbohydrate metabolism
No deterioration in the glycemic and insulinemic
response to glucose load.
No effect on serum lipid concentration.
Safe for long term use
53. Cyperoterone acetate:
A progestin that also has strong antiandrogenic
action.
Inhibits gonadotrophin secretion and interferes with
androgen action on target organs by competing for
androgen receptors
Dosage- 100mg from D5-D14 with ethinyloestradiol
30µg, from D 5 to D25
Side effects: Nausea, fatique, weight gain, loss of
libido, mastalgia
54. Spironolactone:
(Antialdosterone antiandrogenic compound)
Inhibits ovarian and adrenal androgen biosynthesis
Competes for androgen receptors in hair follicle
Inhibits 5 alpha reductase activity
Dosage -100-200mg daily, maintenance dose is 25-50
mg daily
Side effects- fatigue,menstrual irregularities,
hyperkalaemia
55. Finasteride:
5 alpha reductase inhibitor that inhibits conversion of
testosterone to more active 5 alpha hydroxy
testosterone
Dosage- 5 mg daily
56. Flutamide:
Androgen receptor antagonist
Dosage – 100-200mg daily
Side effects - hepatotoxic , Dry skin
Should be combined with a contraceptive
Marked beneficial effect in 6 months
57. Mode of action
Suppress pituitary adrenal axis - suppression of
endogenous ACTH secretion
Use –
In adrenal or mixed adrenal and ovarian
hyperandrogenism
59. Metformin: Antihyperglycemic drug ,in treatment of
hirsutism associated with insulin resistance (e.g. PCOD)
Eflornithine: (13.9% cream)
US FDA approved
It irreversibly inhibits ornithine decarboxylase (ODC), an
enzyme that catalyzes the rate-limiting step for follicular
polyamine synthesis, which is necessary for hair growth.
Improvement occurs gradually over a period of 4-8 weeks
or longer.
Most reported adverse reactions consisted of minor skin
irritation.
60. After 1 – 2years, medication can be stopped to
observe the return of ovulatory cycles.
Even in anovulatory pts, testosterone suppression
continues for 6months to 2 years after
discontinuing treatment
If anovulation persists, return of hirsutism
expected.
How long should treatment be continued?
61. Bleaching - can cause irritation, purities, skin
discoloration
Shaving - Shaving does not lead to worsening of
hirsutism and is a good short-term solution for
facial hair.
- Does not affect the rate or duration of
anagen phase, or diameter of hair
- But yields a blunt tip – illusion of thicker hair
Plucking, Waxing - scarring, folliculitis,
hyperpigmentation
Depilatory creams - Irritant dermatitis
Electrolysis - painful, erythema, inflammation,
scarring
Laser
62. Removal of the source
Adrenal or ovarian tumour – surgically treated
Cushing disease – Adrenalectomy
Radiation to pituitary
Removal of ACTH producing tumor
Iatrogenic cases – Offending drug to be stopped
63. Hirsutism is a symptom of underlying cause
Commonest cause is PCO
Progression may hint to diagnosing tumor
Treatment – Medicines/ Cosmetic