Abnormal hair growth in women (Formerly called Hirsutism) -1) Prevalence of hirsutism is 5-10% of all reproductive age women. PCOS (of all hirsuites 57-82% are due to PCOS) amongst reproductive aged woman in US is about 6-10%. In PCOS both ovarian and adrenal androgen contributes.
2) Causes of hirsutism:- Idiopathic, familial, PCOS women, CAH, HAIR-AN syndrome, Androgen Secreting Tumours of Ovary or Adrenal, Drug intake, above then suggest Cushingoid syndrome
3) Disease 1: PCOS.
4) Disease 4:-Congenital Adrenal Hyperplasia.
Autosomal recessive disorder Different enzymes may be involved. Uncommon in Indians, 21 Hydroxylase deficiency commonest, But 11 β-hydroxylase and 3β-hydroxylae deficiency are possible... All these enzymatic deficiencies cause deficient production of adrenal androsterone, androgen and cortisol. As such production of cortisol and androsterone decreases therefore secretion of ACTH increases leading to hyperplasia of cortical cells. Prevalence 1:1000 person. Classical CAH may case ambiguous ext genitalia.
May be difficult to diagnose CAH from PCOS. Diag: A morning 17-OH-P if above 2 ng/ml then screen test is +ve. Due to 21 Hydroxylase deficiency. If screen +ve then confirmatory test by Inj ACTH (250 mcg) I V. à 30-60 minutes after inj samples are drawn for 17 OHP and Androstenedione. Test is done after overnight fast. If report i.e. Post ACTH is > 10 ng/ml then confirmed CAH-Non Classical Cong Ad Hyperplasia,
What about 11 β-hydroxylase and 3β-hydroxylae deficiency? How to diagnose? ACTH stimulation test wall show excessive production of Androstenedione also.
TR of CAH: - OCP/ Anti-androgens and rarely exogenous Gluco corticoids to suppress Pituitary.
5) Disease 5: Cushing syndrome usually exhibit hirsutism, centripetal obesity, HTN, Striae, Purple cutaneous striae, A 24 hrs urinary free cortisol if four times above the normal then one should consider Cushing’s syndrome. Normal urinary free cortisol is < 150 n. mol/Lit Dexamettasione suppression test:- Screening Test:- 1 mg Dexa at 2300 hrs at nightà serum cortisol on the following morningà if serum cortisol is at 8 a.m. < 50 n. mol/L or < 1.8 mcg/dL may be considered as adrenal suppression.
6) coCortisol in serum, sakiva
7) HAIR-AN syndrome.
Hyperandrogenic Insulin Resistant with Acanthosis Nigricans; - This is an extreme sate of IR. Present in 1-3% of all hyperandrogenic women. Elevated high basal fasting insulin or Glucose medicated excess insulin level. It is akin to more metabolically active form of PCOS.The severity of hyperinsulinaemia is disproportionately MOR than glycaemic profile. The high circulating levels of insulin cause more androgen production in ovarian theca cells.
8) Ovarian and Adrenal Tumours.
9) Idiopathic Hirsuitism.
10) Hyperreaction Luteinalis (pp. 22) - At second or thirdud trimester severe virilization Etiology unknown, but there is some hypersensitivity to HCG à HCG stimulates theca cells to produce more androgens; large ovarian cysts are also seen.
10) What are the androgen dependent areas of the body?
Upper lip, Chin, mid chest, abdomen and back,
11) Time of first appearance- puberty usually,
12) How to evaluate + History Is mens history is suggestive of ovulatory disorders- early menarche, as commonly happens n PCOS, midcycle mucorrhoea, regularity, PMS like s/S Breast tenderness. What is the age of onset and how is the rate of progression of Symptoms? Drug intake?- Danazol, Phenytoin, Cyclosporine, anabolic steroids,
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