EXCESSIVE HAIR GROWTH HIRSUTISM VIRILIZATION. Hair type S Hair type S Lanugo : Body hair seen in...
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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.
Drugs & Exogenous Hormones
variety of drugs decrease SHGB, resulting in increased levels of free T
Androgens
Corticosteroids
Minoxidil
Phenytoin
diazoxide
cyclosporin
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.