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

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EXCESSIVE HAIR GROWTH EXCESSIVE HAIR GROWTH HIRSUTISM VIRILIZATION

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

Page 1: EXCESSIVE HAIR GROWTH HIRSUTISM VIRILIZATION. Hair type S Hair type S Lanugo : Body hair seen in newborn Vellus : Fine adult hair covering body Terminal.

EXCESSIVE HAIR GROWTHEXCESSIVE HAIR GROWTH

HIRSUTISM

VIRILIZATION

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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

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Hair cycleHair cycleSS

• Anagen : Growth influenced by disorders

• Catagen : rapid involution • Telogen : Quiescent

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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

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HIRSUTISM

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

( facial , chest , upper abdominal hair)

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HYPERTRICHOSIS

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

medication such as antiepileptics

Hyperthyroidism

anorexia nervosa

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VIRILIZATION

IN severe pathologic condition , malignancy

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

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androgen levels and quantity of hair growth is not parrarel

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

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EXCESS REPONSIVITY TO ANDROGEN

TESTOSTERONE in target receptors 5-ALPHA –REDUCTASE 1

DIHIDROTESTOSTERONE

Excessive response of receptor to DHT

due to mutation in gene

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ovaries and adrenal glands normally contribute equally to androgen production.

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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.

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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

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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.

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APPROACH TO DIAGNOSIS

Careful historyOnset and progressionFamily historymedicationsPrecocious puberty suggests adrenal enzyme defect

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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

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Evaluation of Hirsutism

1. Total testosterone & or free

2. DHEAS

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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

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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.

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treatment

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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 ?!)

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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

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OcpOcp

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

estrogen-dependent cancers .

relative contraindication smokers hypertension history of migraine

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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

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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.

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FLUTAMIDE :

Blocks the androgen receptors

.liver side effect

KETOCONAZOLE:

• liver toxicity

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Eflornithine cream (Vaniqa)

long-term efficacy remains to be established.