Download Free Medical Hirsutism and Virilization PowerPoint Presentation

Hirsutism and Virilization PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical presentation on Excessive Hairiness (Hirsutism), which is titled "Hirsutism & Virilization", to know about Hirsutism & Virilization, androgen biosynthesis, androgen types, diagnosis, management and treatment of hirsutism and virilization.

Tags : Excessive Hairiness, Hirsutism, androgen biosynthesis, androgen types, diagnosis, management, treatment

Published on : Jul 07, 2021 | Views : 3647 | Downloads : 23

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Unrestricted
Slide 2-

Hirsutism & Virilization Dr.Nasrin Saharkhiz Associate professor SBMU,Dept of Ob&Gyn Beckman2019 CHAPTER 40
Slide 3-

To define: Hirsutism & Virilization To learn Androgen biosynthesis Androgen Types To Diagnosis, management & treat hirsutism & Virilization Objectives
Slide 4-

ppt slide no 4 content not found
Slide 5-

INTRODUCTION Hirsutism is excess terminal hair in a male pattern of distribution. initially by the appearance of midline terminal hair.
Slide 6-

vellus hair is soft, downy, and fine Terminal hair is darker, coarser, and kinkier lanugo hair fine, soft hair of a human fetus
Slide 7-

Origin of excess terminal hair is : Familial pathological
Slide 8-

When a woman is exposed to excess androgens: terminal hair first appears on the: lower abdomen around the nipples next around the chin and upper lip finally between the breasts and on the lower back Usually, a woman with hirsutism also has acne
Slide 9-

ppt slide no 9 content not found
Slide 10-

VIRILIZATION Virilization is defined as masculinization of a woman and is associated with a marked increase in circulating testosterone. as well as hirsutism
Slide 11-

She first notices: enlargement of the clitoris Then: Temporal balding deepening of the voice involution of the breasts remodeling of the limb–shoulder girdle Over time, she takes on a more masculine appearance
Slide 12-

ANDROGEN PRODUCTION Adrenal glands Ovaries Adipose tissue: (extraglandular production of testosterone from androstenedione)
Slide 13-

Three androgens: 1. Dehydroepiandrosterone (DHEA) 2. Androstenedione 3. Testosterone
Slide 14-

1. Dehydroepiandrosterone (DHEA) a weak androgen secreted principally by the adrenal glands generally measured as dehydroepiandrosterone sulfate (DHEA-S) because of its longer half- life, a more reliable measure.
Slide 15-

2. Androstenedione: a weak androgen secreted in equal amounts by the adrenal glands and ovaries.
Slide 16-

3. Testosterone: A potent androgen secreted by: Adrenal glands Ovaries Adipose tissue from the conversion of androstenedione
Slide 17-

dihydrotestosterone (DHT) an androgen more potent than testosterone This metabolic conversion is the result of the local action of 5α-reductase on testosterone within hair follicles and genital skin This is the basis for constitutional hirsutism
Slide 18-

T Androstenedion DHEA Adrenal cortex Ovary %25 %25 %50 %50 %50 %50 %20 %100 %30 DHEAS
Slide 19-

Ovarian androgen production is regulated by luteinizing hormone (LH) In conditions of sustained or increased LH secretion, androstenedione and testosterone increase.
Slide 20-

When androstenedione production increases, there is a dependent increase in extraglandular testosterone production In obese women: conversion of androstenedione to testosterone is increased. increase in estrone
Slide 21-

Testosterone is the primary androgen that causes increased hair growth,acne, and virilization. bound to a carrier protein—sex hormone binding globulin (SHBG) Bound testosterone is unable to attach to testosterone receptors and is metabolically inactive Only a small fraction(1%–3%) of testosterone is unbound (free)
Slide 22-

Testosterone receptors are scattered throughout the body Hair follicles Sebaceous glands Genital skin Some individuals have increased 5α-reductase within hair follicles, resulting in excessive local production of DHT.
Slide 23-

Excess androgen production causes: PCOS Adrenal disorders Testosterone-secreting tumors Iatrogenic Idiopathic causes
Slide 24-

POLYCYSTIC OVARY SYNDROME The most common cause of androgen excess and hirsutism in women The etiology of this disorder is unknown Genetic predisposition Obesity Other causes of LH excess
Slide 25-

Symptoms of PCOS: Oligomenorrhea or amenorrhea Acne,hirsutism Infertility The disorder is characterized by Chronic anovulation Excess androgen
Slide 26-

Definition of PCOS: Rotterdam cr. Two of the following three: Oligo and/or anovulation Clinical or biochemical signs of hyperandrogenism Hirsuitism, acne, or male pattern balding High serum androgens Polycystic ovaries (by ultrasound) Presence of 12 or more follicles in each ovary, measuring 2-9 mm in diameter, or increased ovarian volume
Slide 27-

ppt slide no 27 content not found
Slide 28-

It is also important to rule out other endocrine disorders that can mimic PCOS, such as CAH, Cushing syndrome, and hyperprolactinemia
Slide 29-

Obesity In many women with PCOS, obesity seems to be the common factor (seen in 50% of patients) Stein and Levental first described PCOS patients as women with hirsutism, irregular cycles, and obesity Originally called Stein–Levental syndrome PCOS does not currently have obesity as one of its diagnostic criteria
Slide 30-

PCOS is related to obesity by the following mechanism: LH stimulates the theca lutein cells to increase androstenedione production. Androstenedione undergoes aromatization to estrone within adipocytes. estrone has a positive-feedback action on the pituitary secretion of LH With increasing obesity: increased conversion of androstenedione to estrone. there is coincident increased testosterone production, which causes acne and hirsutism
Slide 31-

In obesity: compensatory hyperinsulinemia result in decreased levels of SHBG more bioavailable circulating androgen stimulus to androgen production in the adrenal gland and ovary Insulin have direct hypothalamic effects: abnormal appetite stimulation and gonadotropin secretion
Slide 32-

Hormonal studies in PCOS (1) increased LH:FSH ratio (2) estrone in greater concentration than estradiol (3) androstenedione at the upper limits of normal or increased (4) testosterone at the upper limits of normal or slightly increased
Slide 33-

The unopposed long-term elevated estrogen increase the risk of: Abnormal uterine bleeding Endometrial hyperplasia Endometrial carcinoma
Slide 34-

Metabolic Syndrome (syndrome X): presence of at least three of the following components: • Waist circumference 35 inches or greater • Triglyceride level 150 mg/dL or higher • High-density lipoprotein cholesterol <50 m/dL • Blood pressure 130/85 mm Hg or higher • Fasting glucose level 100 mg/dL or higher
Slide 35-

Approximately 40% of patients with PCOS have impaired glucose tolerance 8% have overt type 2 diabetes mellitus should be screened for diabetes Hypertension is common Increases the risk of cardiovascular disease
Slide 36-

HAIR-AN Syndrome Acanthosis nigricans has been found in a significant percentage of these patients hyperandrogenism insulin resistance A subgroup of patients with PCOS Administration of the insulin-sensitizing agent metformin in these patients also reduces androgen and insulin levels
Slide 37-

Treatment combination oral contraceptives The most common therapy forPCOS weight reduction ovulation induction - Clomiphene citrate - Aromatase inhibitors: letrozole and anastrozole
Slide 38-

Treatment second-line intervention: - exogenous gonadotropins or - laparoscopic ovarian surgery Insulin sensitizers (metformin alone or with clomiphene citrate) to reduce insulin resistance
Slide 39-

Hyperthecosis A more severe form of PCOS androstenedione production may be so great that testosterone , cause: virilization temporal balding clitoral enlargement deepening of the voice, and remodeling at the limb–shoulder girdle
Slide 40-

often refractory to OCP suppression more difficult to successfully induce ovulation in women with this condition.
Slide 41-

OVARIAN NEOPLASMS Sertoli–Leydig Cell Tumors also called androblastoma and arrhenoblastoma secrete testosterone
Slide 42-

OVARIAN NEOPLASMS Uncommon Virilizing Ovarian Tumors Gynandroblastoma Lipid (lipoid) cell tumors Hillar cell tumors
Slide 43-

ADRENAL ANDROGEN EXCESS DISORDERS The most common are: CAH Cushing syndrome Adrenal neoplasms
Slide 44-

CAH caused by enzyme deficiencies result in precursor excess, resulting in androgen excess DHEA is a precursor for androstenedione and testosterone 21-Hydroxylase Deficiency 11β-Hydroxylase Deficiency
Slide 45-

Manifestations of 21-Hydroxylase Deficiency Severe • Newborn female infant • Virilized (ambiguous genitalia), or virilized and has life-threatening salt wasting Mild • Frequently associated with terminal body hair, acne, alterations in menstrual cycles, and infertility • Patients can also have sonographic evidence of polycystic-appearing ovaries
Slide 46-

Manifested at puberty • Adrenarche may precede thelarche • History of pubic hair growth occurring before the onset of breast development may be a clinical clue
Slide 47-

The diagnosis of 21-hydroxylase deficiency measuring 17-OH progesterone during the follicular phase (preferably fasting) In classic 21-hydroxylase deficiency over 2,000 ng/dL In less severe form: -mildly elevated basal levels, 200 ng/dL -increase to usually 1,000 ng/dL in response to ACTH stimulation DHEA-S and androstenedione elevated
Slide 48-

11β-Hydroxylase Deficiency A less common cause of CAH The clinical features: mild hypertension mild hirsutism The diagnosis: increased plasma desoxycorticosterone
Slide 49-

Treatment of CAH Is aimed at restoring normal cortisol levels Non classic CAH: supplementing glucocorticoids Usually, prednisone 2.5 mg daily (or its equivalent) suppresses adrenal androgen production
Slide 50-

Medical therapy for adrenal and ovarian disorders cannot resolve hirsutism. It can only suppress new hair growth. Hair that is present must be controlled by: shaving Bleaching using depilatory agents electrolysis,or laser hair ablation.
Slide 51-

Cushing Syndrome an adrenal disease resulting in adrenal excess Adrenal neoplasm ACTH-producing tumor signs of corticosteroid excess Truncal obesity Moonlike facies glucose intolerance skin thinning with striae osteoporosis proximal muscle weakness hyperandrogenism , menstrual irregularities
Slide 52-

Adrenal Neoplasms rapid increase in hair growth severe acne amenorrhea sometimes, virilization DHEA-S is usually elevated above 6 mg/mL. The diagnosis: computed axial tomography or MRI Adrenal adenomas must be remove surgically
Slide 53-

CONSTITUTIONAL HIRSUTISM after a diagnostic evaluation, there is no explanation for the cause of the disorder By exclusion The hypothesis: have greater activity of 5α- reductase and therefore, more free testosterone
Slide 54-

Treatment 1-primarily androgen blockade Spironolactone 25 to 100 mg/day is the most commonly used flutamide cyproterone acetate finasteride (5 mg orally daily) Eflornithine hydrochloride 13.9% cream for facial use
Slide 55-

Patients taking an androgen receptor or 5α- reductase blocker should be placed on concomitant oral contraceptives
Slide 56-

2-mechanical removal of the excess hair
Slide 57-

IATROGENIC ANDROGEN EXCESS Danazol Progestin-containing oral contraceptives
Slide 58-

ppt slide no 58 content not found