EXCESSIVE HAIR GROWTH HIRSUTISM VIRILIZATION. Hair type S Hair type S Lanugo : Body hair seen in...

Post on 26-Dec-2015

220 views 0 download

Transcript of EXCESSIVE HAIR GROWTH HIRSUTISM VIRILIZATION. Hair type S Hair type S Lanugo : Body hair seen in...

EXCESSIVE HAIR GROWTHEXCESSIVE HAIR GROWTH

HIRSUTISM

VIRILIZATION

Hair typeHair typeSS

• Lanugo : Body hair seen in newborn

• Vellus : Fine adult hair covering body

• Terminal hair : Thick pigmented hair of scalp and pubic area

Hair cycleHair cycleSS

• Anagen : Growth influenced by disorders

• Catagen : rapid involution • Telogen : Quiescent

Eyebrows , eyelashes , vellus hairs androgen-insensitive

axillary and pubic areas sensitive to low levels of androgens

scalp region androgens cause scalp hairs to spend less time in anagen

HIRSUTISM

EXCESSIVE COARSE (TERMINAL)HAIR. IN PATTERN NOT NORMAL IN FEMALE .

( facial , chest , upper abdominal hair)

HYPERTRICHOSIS

EXCESS NORMAL and NORMAL PATTERN EXCESS NORMAL and NORMAL PATTERN OF DISTRIBUTIONOF DISTRIBUTION

medication such as antiepileptics

Hyperthyroidism

anorexia nervosa

VIRILIZATION

IN severe pathologic condition , malignancy

FRONTOTEMPORAL BALDINGDEPPENING OF VOICE DECREASED BREAST SIZECLITORAL HYPERTROPHY INCREASED MUSCLE MASS AMENORREA / OLIGOMENORRHEA

androgen levels and quantity of hair growth is not parrarel

variability in end-organ sensitivity.Genetic factors ethnic backgrounddark-haired individuals

EXCESS REPONSIVITY TO ANDROGEN

TESTOSTERONE in target receptors 5-ALPHA –REDUCTASE 1

DIHIDROTESTOSTERONE

Excessive response of receptor to DHT

due to mutation in gene

ovaries and adrenal glands normally contribute equally to androgen production.

Gonadal hyperandrogenismPolycystic ovary syndrom insulin resistance SyndromOvarian neoplasm

Adrenal hyperandrogenism

Congenital adrenal hyperplasia (nonclassic and classic)

Cushing's syndromeAdrenal neoplasms

Other endocrine disorders

 Hyperprolactinemia   Acromegaly thyroid dis.

Peripheral androgen overproduction  Obesity  Idiopathic

Pregnancy-related hyperandrogenism  Hyperreactio luteinalis  Thecoma of pregnancy

Drugs  Androgens  oral contraceptives containing androgenic progestins  Minoxidil  Phenytoin  Diazoxide  Cyclosporine

True hermaphroditism

ADRENAL ANDROGEN EXCESS

21 alpha Hydroxylase defieiency11-beta-Hydroxylase deficiency3-beta-dehydrogenase deficiency

*Classical forms usually presented in neonatal period as ambiguous genitalia

*Nonclassic forms are linked with

hirsutism.

APPROACH TO DIAGNOSIS

Careful historyOnset and progressionFamily historymedicationsPrecocious puberty suggests adrenal enzyme defect

Physical Exam

• Hair pattern type,distribution ,quantity (F&G)

• acne• Virilization

• Cushingoid features, galactorrhea , acromegal…

• Acanthosis nigricans (in PCOS)• Wt , ht , BP

• Tanner staging

• Ovarian masses

Evaluation of Hirsutism

1. Total testosterone & or free

2. DHEAS

DHEAS

adrenal source CAH or Cushings

T , DHEA-S normal or minimally elevated

Ovarian source Pelvice U/S r/o tumor

Rapid Onset Virilization T>2ng/mL

indicate ovarian neoplasm

A baseline plasma total testosterone level (>3.5 ng/mL) usually indicates a virilizing tumor(>2 ng/mL) is suggestive. nl=1

A basal DHEAS level (>7000 µg/L) nl=2500suggests an adrenal tumor.

CT or MRI for adrenal mass. ultrasound may help to identify an ovarian mass.

treatment

ManagementEstrogen effective 20%

• Reduces LH so ovarian androgen

• increased SHBG

• competition at the cellular level for binding to androgen receptor

• lower DHEA ( with lower ACTH ?!)

Progestins vary in suppressive effect on SHBG levels so in androgenic potential.

Ethynodiol diacetate low androgenic potential

Norgestimate nonandrogenic.

Drospirenoneanalogue of spironolactone (anti mineralocorticoid) & antiandrogenic

OcpOcp

contraindicated• history of thromboemboli • increased risk of breast or other

estrogen-dependent cancers .

relative contraindication smokers hypertension history of migraine

SIPRONOLACTONE:

• Androgen receptors• Androgen biosynthesis• metabolic clearance of teststerone ( Testosterone Estrogen )

Spironolactone + OC is well established regimen

BP low, K low, female feature in male fetus , irregular mens

Cyproterone acetate

•Competitive inhibition of binding testosterone and DHT to androgen receptor.

•Clearance of testosterone by inducing hepatic enzymes

Cyproterone (50 to 100 mg) is given on days 1 to 15 and ethinyl estradiol (50 µg) is given on days 5 to 26 of the menstrual cycle.

Side effects: irregular uterine bleeding, nausea, headache, fatigue, weight gain, and decreased libido.

FLUTAMIDE :

Blocks the androgen receptors

.liver side effect

KETOCONAZOLE:

• liver toxicity

Eflornithine cream (Vaniqa)

long-term efficacy remains to be established.