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APGO educational topic number 44
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hirsutism and viralization hirsutism
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occurs in 7% of women it has an
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estimated economic burden of 600 million
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dollars annually hirsutism and
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viralization can cause significant
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emotional distress for our patients the
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objectives are to recognize normal
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variations and abnormalities in
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secondary sexual characteristics to
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define hirsutism and viralization
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describe the pathophysiology and
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identify ideologies of hirsutism
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describe the steps in the evaluation and
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initial management options for hirsutism
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and realization and finally describe how
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hirsutism and viralization are
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manifested in other medical disorders
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let’s start with some basic definitions
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of hirsutism and viralization hirsutism
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is accessed terminal hair in a male
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pattern of distribution terminal hair is
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dark and coarse versus vellus hair which
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is soft downy and fine prior to puberty
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all hair is vellus when androgen levels
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rise during puberty Bella’s follicles
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and specific areas of the body develop
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into terminal hairs with hirsutism
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terminal hair first appears on the lower
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abdomen around the nipples chin and
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upper lip pictorial scale such as the
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pheromone Galway scale have been created
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to help objectify normal versus abnormal
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amounts of hair growth
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each of the nine body areas most
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sensitive to androgen are assigned a
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score from 0 of no hair to 4 of frankly
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virile these are some to provide a
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hormonal hirsutism score it is important
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to note that different ethnic groups
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will have different amounts of normal
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hair growth and distributions some
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experts have recommended using the term
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patient important hirsutism to indicate
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symptoms that are causing patient
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distress hirsutism causes 50% are
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idiopathic which will be often
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constitutional or familial polycystic
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ovarian syndrome or PCOS is the most
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common pathological cause other causes
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include congenital adrenal hyperplasia
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viralization refers to masculinization
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of a woman woman will present with
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enlargement of the clitoris temporal
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balding deepening of the voice
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involution of the breasts and remodeling
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of the limb shoulder girdle let’s now
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move to androgen production women there
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are three primary androgens that are
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Purdue
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and women dehydroepiandrosterone or DHEA
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androstenone and testosterone these are
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produced by the adrenal glands ovaries
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and peripheral tissues DHEA is primarily
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secreted by the adrenal glands and
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ovaries let’s very quickly revisit the
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cortisol synthesis pathway remember that
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in the adrenal gland cholesterol is
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converted to aldosterone and cortisol
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DHEA is one of the precursor hormones in
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this pathway we’ll go back to this
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cortisol synthesis pathway later in the
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video
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going back to our three primary antigens
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Andres team diode is equally secreted by
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the adrenal glands and the ovaries
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testosterone is a potent androgen that
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are secreted from the adrenal glands
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ovaries and from peripheral tissues
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testosterone is the primary androgen
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that causes increased hair growth and
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physical changes associated with varial
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is asian let’s now move on to etiology
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x’ for androgen excess polycystic
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ovarian syndrome or PCOS is the most
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common pathological cause for women
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presenting with hirsutism remember that
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this is a clinical diagnosis the
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diagnosis involves menstrual
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irregularity clinical or biochemical
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signs of hyperandrogenism polycystic
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ovaries on ultrasound here is a classic
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polycystic ovary with the small
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follicles around the periphery of the
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ovary measuring less than 9 millimeters
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this is referred to as the ring of
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pearls different organizations have
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different criteria for the diagnosis of
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PCOS but most groups endorse the
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diagnosis can be made if a patient has
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two out of three of these criteria there
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should also be exclusion of other causes
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of androgen excess or ovulatory
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disorders polycystic ovarian syndrome is
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often associated with obesity and many
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women will describe at the acquisition
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of body fat coincides with the onset of
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PCOS symptoms women will describe
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situations such as changing to a
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sedentary job gaining weight in college
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or having a baby
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why is PCOS related to obesity remember
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that the pituitary gland secretes LH
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which stimulates the collodial cells in
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the ovary to produce androstenone
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in adipose tissue this and resting
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Dioner is converted to ester own which
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is a weak estrogen which positively
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stimulates the pituitary to secrete more
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LH the increased la stimulation leads to
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more
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éand I own the androstenone is converted
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testosterone which leads to acne and
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hirsutism I think the important thing to
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remember is that Esther Owen is a
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positive stimulator of LH let’s move now
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to more uncommon causes of
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hyperandrogenism congenital adrenal
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hyperplasia accounts for 1.5 to 2.5
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percent of women with hyperandrogenism
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these enzyme deficiency disorders caused
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substrate access which result in
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androgen excess here again is our
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simplified version of the cortisol
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synthesis pathway cholesterol is
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converted to aldosterone and cortisol
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a21 hydroxylase deficiency or 11 beta
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hydroxylase deficiency will lead to
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increased levels of DHEA for this is one
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of the substrates in the pathway a very
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neoplasms are rare causes of high
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androgen levels accounting for
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approximately 0.2 percent of women with
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hyperandrogenism sertoli lytic tumors
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are a very neoplasms that secrete
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testosterone these tumors constitute
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0.4% of ovarian tumors they usually
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occur in women between the ages of 20
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and 30 and women will describe rapid
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onset of acne hirsutism amenorrhea and v
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realization other medical conditions to
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include on the differential diagnosis of
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high androgen levels include Cushing’s
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syndrome hyperprolactinemia acromegaly
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and thyroid dysfunction let’s move now
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to evaluation of hirsutism first start
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with a careful history assess how
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rapidly the symptoms have developed for
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our rapid pace of development should
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raise concerns about an androgen
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secreting neoplasm the high frequency of
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polycystic ovarian syndrome warrants
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attention to menstrual irregularity ask
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about viralization symptoms such as
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voice changes and ask about the hair
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patterns of family members remember to
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ask about medications and supplements as
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well on physical examination a faraman
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Gallwey score should be calculated and
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make sure to perform an abdominal and
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bimanual examination to assess for
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abdominal and pelvic tumors and a
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careful skin examination to check for
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acne striae or acanthosis nigricans in
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addition make sure to look for a
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realization sign such as enlargement of
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the clitoris temporal balding or
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involution of the breasts the history
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and physical examination can help you
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determine if the patient is low moderate
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or high risk of having an androgen
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secreting tumor
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for a low-risk patient therapy can be
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initiated with a six-month trial of
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hormonal therapy such as oral
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contraception for moderate to high risk
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patients hormonal evaluation and imaging
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should be ordered further workup to
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consider includes thyroid function tests
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prolactin and 17 hydroxy progesterone
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levels for further evaluation for other
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medical ideologies of hyperandrogenism
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let’s conclude by discussing treatment
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hair removal methods include bleaching
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shaving epilation which is waxing or
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plucking electrolysis or laser
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pharmacologic measures include a floor
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nathan hydrochloride which is a cream
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which has recently been approved for the
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treatment of facial hirsutism oral
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contraception works by suppressing
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plasma testosterone levels by inhibiting
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ovarian function and finally the
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anti-androgen medications of
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spironolactone and finasteride this
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concludes the app go video on hirsutism
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and viralization we’ve defined important
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terms described pathophysiology and
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described steps in the evaluation and
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initial management of these conditions
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