Speaker 1: All right, so let's talk about polycystic overy syndrome before
Speaker 1: we get started. As always, thank you so much for
Speaker 1: the support, Thank you, thank you so much. All Right,
Speaker 1: let's talk about polycystic ovary syndrome or p COS as
Speaker 1: I like to call it, So polycystic overy syndrome. The
Speaker 1: name quite literally means a syndrome of many cysts of
Speaker 1: the ovaries. So you might think that that's all this is,
Speaker 1: but in actuality, you don't even need to have polycystic
Speaker 1: overies to be diagnosed, and the fluid filled structures in
Speaker 1: the ovaries they're not even true cysts, but we'll talk
Speaker 1: more about that later. So PCOS is one of the
Speaker 1: most common endochronopothies in women of reproductive age. It effects
Speaker 1: between six point five and ten percent of all women
Speaker 1: of reproductive age. Let's go ahead and get started with
Speaker 1: the patho first. So the patho is pretty complex, multifactorial,
Speaker 1: there's a lot going on, so we'll keep it focused
Speaker 1: on what you need to know. Some key concepts or
Speaker 1: trends that we typically see in patients with piacos. So
Speaker 1: starting with your LH levels. So PACOS patients have altered
Speaker 1: LH levels with relatively higher serum lutinizing hormone concentrations relative
Speaker 1: to FSH concentrations. This is just a small component of
Speaker 1: the whole picture, but I think is important to understand.
Speaker 1: So let's do a quick review of a normal functioning
Speaker 1: hypothalamic pituitary ovariant axis. In a normal HPO axis, the
Speaker 1: hypothalamus releases GnRH in a pulsatile manner, stimulating the anterior
Speaker 1: pituitary to secrete LH and FSH. LH goes down and
Speaker 1: acts on the thika cells in the ovary, promoting androgen
Speaker 1: production primarily androstendon, while FSH stimulates granulosa cells to produce aromatase.
Speaker 1: Romatase is an enzyme that converts these androgens into estrogen,
Speaker 1: specifically estradil. So as this process goes on, a dominant
Speaker 1: follicle develops. F SH stimulates the follicle to develop. Rising
Speaker 1: estrogen levels trigger positive feedback on the pituitary, leading to
Speaker 1: a surge in LH, which induces ovulation. Most of this
Speaker 1: you probably already know. After ovulation, progesterone from the corpus
Speaker 1: lutium provides negative feedback, slowing down GnRH pulses, reducing LH
Speaker 1: and FSH secretion to complete the cycle. It's a lot,
Speaker 1: but here's the part that you need to know and
Speaker 1: p cosse. This balance is disrupted due in part two,
Speaker 1: a higher pulsatile frequency of g n rh which LH
Speaker 1: is more responsive to, leaving us with excessive amounts of
Speaker 1: LH relative to f SH levels. So it means those
Speaker 1: thikas cells which are stimulated by LH are now producing
Speaker 1: too many androgens and FSH can't keep up to convert them.
Speaker 1: These elevated androgen levels, along with the relatively lower f
Speaker 1: SH levels, which normally stimulate follicular development, impair normal follicle maturation,
Speaker 1: resulting in anovulation and in accumulation of these immature follicles
Speaker 1: in the ovary, which lead to the classic appearance we'll
Speaker 1: see on ultrasound in some patients. Okay, so remember the
Speaker 1: increased LH to FSH ratio. One other part of the
Speaker 1: pathway I feel is important to understand is how insulin
Speaker 1: resistance plays a role. So fifty to seventy percent of
Speaker 1: females with p costs demonstrate clinically measurable insulin resistance, So
Speaker 1: we have insulin resistance which leads to compensatory hyper insulinemia.
Speaker 1: So high levels of insulin in the body. But what
Speaker 1: do high levels of insulin have to do with androgen
Speaker 1: excess and ovulatory to spunction. Well more than you'd think,
Speaker 1: So besides the obvious regulation of glucose that comes to
Speaker 1: mind when thinking of insulin, it does something else when
Speaker 1: in high levels, and that is to stimulate the THIKA
Speaker 1: cells of the ovaries to produce more androgens. So kind
Speaker 1: of like what we were talking about before with the
Speaker 1: effect of LH on the ovaries, insulin can stimulate steroidogenesis,
Speaker 1: causing those THECA cells to crank out more androgens. And
Speaker 1: these increased levels of insulin also inhibit production of something
Speaker 1: known as SHBG, sex hormone binding globulin. This is a
Speaker 1: transport protein that binds to hormones like testosterone as well
Speaker 1: as others, and it regulates their access to certain tissues.
Speaker 1: When hormones like testosterone are bound to SHBG, though, and
Speaker 1: this is the important part, these hormones are rendered inactive,
Speaker 1: meaning they can't do anything. So the fact that these
Speaker 1: high insulin levels inhibit production of SHBG means we have
Speaker 1: more of those androgens hanging out free in the bloodstream
Speaker 1: in their active state, able to unleash their hyper androgenic effects.
Speaker 1: High insulin levels even seem to override the ovara's natural
Speaker 1: resistance to LH, making them hyperresponsive, driving even more androgen production,
Speaker 1: all of which lead to some of the clinical manifestations
Speaker 1: will go over all. Right, So that's a lot of info.
Speaker 1: May take away. Excess LH relative to FSH, excess insulin
Speaker 1: from insulin resistance. Remember those and let's move on to
Speaker 1: the clinical manifestations next. So this is a syndrome, so
Speaker 1: the clinical presentation can vary from person to person, and
Speaker 1: there's many potential clinical manifestations irregular menstrual cycles, hersutism, acne, obesity,
Speaker 1: mood disorders, metabolic issues, cardiovascular issues, diabetes. But the two,
Speaker 1: the two I want you to remember that are also
Speaker 1: part of the diagnostic criteria will go over shortly is
Speaker 1: as follows. The first is menstrual dysfunction oligomenareea amenareea. So
Speaker 1: women with PA costs will have infrequent or absent menstrual cycles,
Speaker 1: which is caused by infrequent or absent ovulation. As a result.
Speaker 1: Infertility is a common consequence of these menstrual regularities and
Speaker 1: is frequently one of the reasons women with pea costs
Speaker 1: will seek medical attention. So remember oligomenarea or amenarea and
Speaker 1: the potential for infertil Next, hyper androgenism, hersaitism, acne, female
Speaker 1: pattern hair loss. So these are the repercussions of those
Speaker 1: excess androgens like testosterone we mentioned earlier. So hersaitism which
Speaker 1: is a thick or pigmented body hair also known as
Speaker 1: terminal hair and a male distribution pattern. So we can
Speaker 1: see dark hair growth on the upper lip, the chin,
Speaker 1: around the nipples, the perieriolar surface, as well as the
Speaker 1: lower abdomen. The linear alba acne is common as well.
Speaker 1: This can be on the face, back, chest as well
Speaker 1: as other areas of the body. And then finally, female
Speaker 1: pattern hair loss, so these women may start to have
Speaker 1: thinning of the hair on their head. This diffuse alopecia. Okay,
Speaker 1: So menstrual dysfunction, oligo or a menorrhea, and hyper androgenism.
Speaker 1: Now these are the two I want you to focus on,
Speaker 1: but of course be aware there are other potential clinical
Speaker 1: manifestations metabolic issues like obesity, insulin resistance, but focus on
Speaker 1: the menstrual dysfunction, infertility and hyper androgenic features. Let's talk
Speaker 1: about diagnosis next. So when we're talking about the diagnosis
Speaker 1: of PECOS, there is no no single lab or imaging
Speaker 1: study you can do to definitively diagnose this syndrome. So
Speaker 1: what we do to make the diagnosis is by using
Speaker 1: something known as the Rotterdam criteria. There are a few
Speaker 1: different criteria out there, but the Rotterdam criteria is the
Speaker 1: one most expert groups use and therefore it's the one
Speaker 1: you need to know. So what does the criteria entail?
Speaker 1: So to make the diagnosis of PA costs, you need
Speaker 1: to have two out of the three based on the
Speaker 1: Rotterdam criteria. The first is oligoovulation or anovulation, which will
Speaker 1: generally manifest with menstrual regularity like we talked about before,
Speaker 1: so infrequent or absent menstrual cycles. The next is clinical
Speaker 1: and or biochemical signs of hyper androgenism. So this means
Speaker 1: either the patient has clinical signs of hyperandrogenism so hersitism,
Speaker 1: actne et cetera. Or they have biochemical signs of hyper
Speaker 1: androgenism so you obtain labs and they have elevated testosterone levels.
Speaker 1: And then finally, the last criteria, which we haven't talked
Speaker 1: too much about yet is the ultrasound defindings. So the
Speaker 1: last criteria is polycystic ovaries by ultrasound. So let's talk
Speaker 1: about the ultra findings. Like I mentioned before, the fluid
Speaker 1: filled structures in the ovary that we see in some
Speaker 1: women with PA costs are not cists, but rather these
Speaker 1: immature follicles that never developed during those failed ovulation events.
Speaker 1: So an ultrasound will see abnormally high numbers of small
Speaker 1: follicles within these enlarged sclerotic ovaries. The small follicles are
Speaker 1: often located on the periphery of the ovary and sometimes
Speaker 1: they'll resemble a string of pearls and you'll sometimes hear
Speaker 1: them being referred to as that string of pearl sign
Speaker 1: when describing p COS ultrasound findings. So the Rotterdam criteria
Speaker 1: states a positive finding on ultrasound is twelve or more
Speaker 1: of these small follicles and either ovary measuring two to
Speaker 1: nine millimeters in diameter and or increased ovarian volume over
Speaker 1: ten mL. Now, there are some groups that suggest revising
Speaker 1: this increasing to twenty or more follicles per ovary because
Speaker 1: of the improvements and resolution of pelvic ultrasound and the
Speaker 1: fact that a percentage of normal cycling women met the
Speaker 1: threshold without having PA costs. What that means to you is,
Speaker 1: don't memorize these numbers. If they can't agree on the
Speaker 1: criteria for the specifics here, they can't expect you to
Speaker 1: remember them or memorize that for an exam. So don't
Speaker 1: worry so much about the specific number. But keep in mind,
Speaker 1: if the question is describing numerous small follicles and a
Speaker 1: big old plump ovary, they're probably describing pea cos all right.
Speaker 1: So that's the Rotterdam criteria. That's what you need to know.
Speaker 1: Irregular ovulation, hyper androgenism, and polycystic ovaries on ultrasound you
Speaker 1: need two out of a three, meaning if you have
Speaker 1: a patient with irregular mensis and hyper androgenic symptoms, you
Speaker 1: don't even need an ultrasound to diagnose. But there is
Speaker 1: one last part we're missing, one very important component. Before
Speaker 1: you make the diagnosis based on the Rotterdam criteria, you
Speaker 1: absolutely have to rule out your differentials. Rotterdam criteria also
Speaker 1: require exclusion of other conditions that mimic pea costs, So
Speaker 1: peacos has some very sneaky impostors conditions that have many
Speaker 1: of the same or in some cases exactly the same
Speaker 1: clinical findings. So once you establish a patient fits the
Speaker 1: Rotterdam criteria, the next step is to rule out your
Speaker 1: very important differentials. Now, there are a number of differentials.
Speaker 1: I'm not going to cover every single one, but the
Speaker 1: ones you need to know and the ones that will
Speaker 1: likely be tested on can all be found in your apartment.
Speaker 1: Your apartment as an APT what does that mean? Apartment
Speaker 1: APT stands for three important areas and those are adrenal, pituitary,
Speaker 1: and thyroid. So these are the differentials to roll out
Speaker 1: before making your diagnosis, and they can all be found
Speaker 1: in your apartment. So starting with adrenal, the letter A,
Speaker 1: what I'm going to cover right now is the most
Speaker 1: important differential you need to know, and if they're going
Speaker 1: to give you a differential on an exam, it will
Speaker 1: very likely be this one. This is known as NCCAH
Speaker 1: non classic congenital adrenal hyperplasia. If you want to forget
Speaker 1: all of the other differentials, I'm going to go over
Speaker 1: and just remember one. This is it. A patient with
Speaker 1: NCCAH can present with almost identical signs and symptoms as
Speaker 1: those with PECOS hyperindrogenism, olligo, manaia, polycystic overies, So you
Speaker 1: don't want to miss this. So to screen for this,
Speaker 1: you obtain a serum seventeen hydroxy progesterone, which is also
Speaker 1: super high heal to know, I sometimes remember the as
Speaker 1: apartment seventeen just to help me remember this screening test
Speaker 1: because it's just so popular to be tested on, and
Speaker 1: I definitely got a question on this in school, So
Speaker 1: please remember this one and then the other. Adrenal differential
Speaker 1: is an adrenal tumor, so a patient with an adrenal
Speaker 1: androgen secreting tumor or an adrenal cortical carcinoma. These patients
Speaker 1: can have clinical and biochemical manifestations of hyper androgenism like
Speaker 1: pa COS, but generally more severe. These patients usually have
Speaker 1: significant elevation of testosterone and or DHVAS levels way higher
Speaker 1: than PECOS patients, and usually will exhibit more severe signs
Speaker 1: of hersitism and even signs of virilization things like cliteromegaly,
Speaker 1: increased muscle mass, and deepening of the voice, which we
Speaker 1: typically don't see in pea COS. Okay, so that's the
Speaker 1: a for apartment. Adrenal main takeaway, don't forget NCCAH screened
Speaker 1: with the seventeen hydroxy progesterone. Remember your apartment seventeen. Next
Speaker 1: letter in the apartment is P which stands for pituitary. Specifically,
Speaker 1: we're talking about hyper prolactinemia. So hyperperlactinemia, which is an
Speaker 1: elevation of prolactin levels from the pituitary, can lead to infertility,
Speaker 1: oligomenarea or a menareea, so this needs to be in
Speaker 1: your workup. And then finally, the T stands for thyroid,
Speaker 1: so both hypo and hyperthiroidism can also lead to oligomenarea,
Speaker 1: so check a TSH as well. There are, of course
Speaker 1: other differentials Cushing syndrome, primary ovarian insufficiency, ovarian hyperthiicosis, pregnancy
Speaker 1: of course a very important cause of a menarea. But
Speaker 1: the ones I highlighted in your apartment those are the
Speaker 1: ones to remember as those will likely be tested on again.
Speaker 1: Highlighting non classic congenital adrenal hyperplasia, which you screen for
Speaker 1: with a seventeen hydroxy progesterone. All right, next, let's talk
Speaker 1: about treatment. So treatment for PCOS is targeted at a
Speaker 1: number of different areas because of all of the complications
Speaker 1: associated with this condition. Remember we have oligomanarea, hyperindrogenism and fertilities, obesity,
Speaker 1: insulin resistance, dyslibidemia. So I'm breaking this down to highlight
Speaker 1: the essentials. Let's start with what is considered the first
Speaker 1: line intervention for many women with peacos, and that is
Speaker 1: lifestyle changes diet exercise, weight reduction. Specifically in our overweight
Speaker 1: or obese patients with p costs, Diet, exercise and weight
Speaker 1: loss are very effective for improving insulin resistance, decreasing the
Speaker 1: hyperandrogenic symptoms, and some studies have found that modest weight
Speaker 1: loss five to ten percent reduction in body weight may
Speaker 1: restore normal ovulatory cycles and improve pregnancy rates. Of course,
Speaker 1: this is also beneficial for managing the underlying metabolic abnormalities
Speaker 1: we talked about cardiovascular disease, type two diabetes, etc. So
Speaker 1: this should be the first step for all overweight and
Speaker 1: obese women with PA costs. The next step for treatment
Speaker 1: we're going to talk about. Our medications are pharmacologic therapy.
Speaker 1: We're going to break this down into two categories, women
Speaker 1: pursuing pregnancy and those who are not pursuing pregnancy. So
Speaker 1: starting first with women not pursuing pregnancy, a patient who
Speaker 1: does not want to get pregnant, who has menstrual dysfunction
Speaker 1: and or androgen excess, which medication can we use? So
Speaker 1: the first line pharmacotherapy for most women will be with
Speaker 1: a combined oral contraceptive or a COC, which is a
Speaker 1: combination of estrogen and progestin. So the coeocs have a
Speaker 1: number of benefit for women with PCOS. First, they suppress
Speaker 1: ovarian androgens, decreasing the hyper androgenic features. Obviously, provide contraception
Speaker 1: because even women with oligomenarrhea may still ovulate intermittently lead
Speaker 1: to unwanted pregnancy. And then finally, something that we may
Speaker 1: not be thinking about, but patients with chronic annovulation like
Speaker 1: in PECOS. These patients are at higher risk for endometril
Speaker 1: hyperplasia and even endometrial cancer. And that's because we have
Speaker 1: this chronic anovulatory state causing the endometrium to be exposed
Speaker 1: to estrogen without the balancing effect of progesterone. We call
Speaker 1: this unopposed estrogen, and combined oral contraceptives help prevent this
Speaker 1: by providing daily progestin, which is a synthetic form of
Speaker 1: progesterone which counteracts the proliferative effects of estrogen on the
Speaker 1: endometrium and the second part of the combined oral contraceptive,
Speaker 1: the estrogen component reduces serum androgen concentrations by increasing SHBG concentration.
Speaker 1: Remember SHBG the guy who gives testosterone a big hug
Speaker 1: and doesn't let go. So this in turn reduces the
Speaker 1: symptoms of acne or hersitism. Binding these in a CEOC
Speaker 1: helps you manage both hyper androgenism and menstrual dysfunction, and
Speaker 1: that's why these are generally considered first line pharmacologic treatment. Now,
Speaker 1: what about a patient with hyperandrogenic symptoms who's been on
Speaker 1: a COEC for many months with no improvement. What other
Speaker 1: medication do we have in our arsenal specifically for these
Speaker 1: persistent hyperandrogenic symptoms. Well, the one you should know is spirinolactone.
Speaker 1: Spiralactone is a minerali cordiicoid receptor antagonist, and it is
Speaker 1: an effective treatment option for androgen excess as it blocks
Speaker 1: androgen receptors and also decreases testosterone production. And spirinalactone falls
Speaker 1: under the women not pursuing pregnancy category because you do
Speaker 1: not want to get pregnant while taking this medication as
Speaker 1: it can actually feminize male fetuses, preventing development of their genitalia,
Speaker 1: so the patient needs to also be on a contraceptive
Speaker 1: while taking this medication. There are some other options out there,
Speaker 1: such as finess, dride fluta, mind, but spirinalactone is the
Speaker 1: preferred agent compared to the other available options due to
Speaker 1: its efficacy. All right, next, let's talk about women who
Speaker 1: are pursuing pregnancy who are experiencing infertility and require treatment.
Speaker 1: So before we go over our meds and ovulatory women
Speaker 1: with peacos who are overweight oral beats should attempt to
Speaker 1: weight loss prior to initiating ovulation induction therapy. In most cases,
Speaker 1: some older women or women whose testing shows diminished ovarian
Speaker 1: reserve sometimes they'll go straight to meds, but in general
Speaker 1: weight loss for navulatory women who are overweight oral beese
Speaker 1: weight loss is recommended first. If lifestyle changes and weight
Speaker 1: loss are not effective and medication is needed, the one
Speaker 1: you should know is in romatase inhibitor by the name
Speaker 1: of lectrisol. Lectrosols should be first line treatment for ovulation
Speaker 1: induction in infertile analvieslory women with peacos. Now this has
Speaker 1: shifted over the years, as clomaphene used to be first
Speaker 1: line by per up to date and the twenty eighteen
Speaker 1: International evidence based guidelines, lectrosol is now the first line
Speaker 1: treatment option for ovulation induction in women with peacos, Like
Speaker 1: a number of pea cost treatments. It's still not FDA
Speaker 1: approved for the syndication, so your patients need to be
Speaker 1: aware of that, And there are some alternatives clomaphene met foreman,
Speaker 1: although both of those are less effective for live birth
Speaker 1: rates compared to lectrozol, so I would just focus on
Speaker 1: lectrosol after weight loss in women pursuing pregnancy. So how
Speaker 1: does letrozol work for ovulation induction? While letrozol is in
Speaker 1: aromatase inhibitor. Romatase, as we briefly discussed earlier during the
Speaker 1: path or review, is an enzyme that converts androgens into estrogen.
Speaker 1: So if we inhibit aromatase, less endrogens are converted to
Speaker 1: estrogen and we have much less estrogen in the body.
Speaker 1: When we have less estrogen in the body, the hypothalamus
Speaker 1: and pituitary sense this say oh, crap we need to
Speaker 1: help out, and they produce more FSH, that hormone we
Speaker 1: have been lacking because LH took over the show, and
Speaker 1: with more FSH we have improved follicular development and improved
Speaker 1: ovulatory rates. Those are the mens I think you should know.
Speaker 1: There's plenty of others, but the ones I went over
Speaker 1: are the most commonly used and the ones you'll likely
Speaker 1: get tested on. All right, so that is p COS.
Speaker 1: It's a lot, so you probably need a mnemonic. Now,
Speaker 1: before I tell you what the mnemonic is, I first
Speaker 1: want to be clear. This is just a memory tool.
Speaker 1: It's just a way to remember what you need to
Speaker 1: know about pa cos. In no way do I intend
Speaker 1: for this to be offensive to anyone with PCUS. It's
Speaker 1: just a simple little visualization that helped me remember. So
Speaker 1: PCUS or pa COS I used to remember in Seat
Speaker 1: of Peacos as pea clause. Piacos is pea clause as
Speaker 1: in Santa Claus, and Santa Claus contains all of the
Speaker 1: high old things you need to know about peacos, including
Speaker 1: a Rotterdam criteria and the most important meds. So again,
Speaker 1: PACs is now pea clause as in Santa Claus. So
Speaker 1: when we visualize our Pea cos Santa Claus, you'll notice
Speaker 1: a few things about this version of him. First, in
Speaker 1: his right hand, he's holding a ball of lettuce, a
Speaker 1: lettuce ball. His left hand, he's holding a bottle of
Speaker 1: Coca Cola. On his forehead is a big old pimple
Speaker 1: being popped with a spear. He's wearing a pearl necklace
Speaker 1: on the wall as a calendar with December twenty fifth circle,
Speaker 1: and of course has expected he has a big white beard,
Speaker 1: as we've all come to know him for now, what
Speaker 1: do all these things represent when it comes to Peacas. First,
Speaker 1: that ball of lettuce in his right hand, That lettuce
Speaker 1: ball helps remember the first line pharmacologic therapy for patients
Speaker 1: pursuing pregnancy letrasol lettuce ball letrasol. And his left hand
Speaker 1: holds the clue for first line treatment for women not
Speaker 1: pursuing pregnancy, COC's or combined oral contraceptives with the first
Speaker 1: three letyers of Coca Cola highlighted coc What about the
Speaker 1: big pimple on his forehead being popped by a spear.
Speaker 1: Pimple represents your hyper androgenic symptoms like acne and the
Speaker 1: spear popping it helps you remember how you treat it
Speaker 1: speir in a lactone, spear rhonolacton, speierronolactone. The anti androgen
Speaker 1: we used for patients with persistent hyperandrogenic symptoms despite coc monotherapy,
Speaker 1: is why beard helps you remember the hersaitism we can
Speaker 1: see in patients with peacos. The pearl necklace helps you
Speaker 1: remember the string of pearl sign remember those numerous follicles
Speaker 1: on the periphery of the ovary. And then the calendar
Speaker 1: on the wall shows December twenty fifth circled, symbolizing infrequent
Speaker 1: or aps in periods like Sanna who only shows up
Speaker 1: once a year in his red suit. So there's a
Speaker 1: lot to remember in peacos. But I feel like if
Speaker 1: you can just remember Sanna and Apartment seventeen cement this
Speaker 1: crazy image in your brain, you should be just fine.
Speaker 1: Now that we have our mnemonic, let's do a few
Speaker 1: quick questions to test your knowledge. Question one, a twenty
Speaker 1: nine year old woman presents to the office complaining of
Speaker 1: excessive hair growth on her upper lip, chin, lower abdomen,
Speaker 1: as well as irregular menstrual cycles. The patient is five
Speaker 1: feet five inches tall, weighs one hundred and thirty two pounds,
Speaker 1: and has a BMI of twenty two. On physical examination,
Speaker 1: there is terminal hair noted on the face and along
Speaker 1: the line alba of the lower abdomen. She's not currently
Speaker 1: taking any medications, denies any known medical conditions, and is
Speaker 1: not planning on pregnancy at any point in the near future.
Speaker 1: She's interested in starting a medication to address the persistent
Speaker 1: hair growth on her face and abdomen and the absence
Speaker 1: of contraindications. Which of the following would be the most
Speaker 1: appropriate next step in management for the likely diagnosis A
Speaker 1: letrazol B spirriinalactone C met foreman D combined oral contraceptive
Speaker 1: or E lifestyle changes, diet, exercise, weight reduction. So the
Speaker 1: correct answer is D combined oral contraceptive. So why is
Speaker 1: that the correct answer? So we have a twenty nine
Speaker 1: year old female presenting with hersaitism or regular metro cycles
Speaker 1: based on the Rotterdam criteria. She has pics. Of course,
Speaker 1: to definitively say that full work up to roll out
Speaker 1: your differentials would be needed, but that's not what this
Speaker 1: question is asking. It's asking based on the likely diagnosis
Speaker 1: which treatment are you going to recommend to her hyper
Speaker 1: androgenic symptoms? So we know the medication we're going to
Speaker 1: prescribe as a coc or combined oral contraceptive. Remember that
Speaker 1: bottle of Coca Cola and Santa's left hand. Now, what
Speaker 1: about the other options? While letrozol would not be appropriate,
Speaker 1: this medication is used for ovulation induction in women pursuing pregnancy.
Speaker 1: Spirinalactone could be used as an adjunct therapy for persistent
Speaker 1: hyperandrogenic symptoms, but it's generally not first line met foreman
Speaker 1: which at one time was used pretty frequently for peacs,
Speaker 1: is no longer recommended for hersaitism per the twenty eighteen
Speaker 1: Endercin Society guidelines, as it has been found to provide
Speaker 1: little or no benefit. And then finally, lifestyle would have
Speaker 1: been appropriate if this patient was overweight or obese, but
Speaker 1: this patient as a normal BMI of twenty two. Question two.
Speaker 1: A twenty six year old woman presents to the clinic
Speaker 1: with concerns about difficulty becoming pregnant. She and her partner
Speaker 1: have been trying to conceive for several months without success.
Speaker 1: She reports only one to two menstrual cycles over the
Speaker 1: past year. It's not on any medications and has no
Speaker 1: significant past medical history. Physical examination reveals hersatism on the
Speaker 1: upper lip and lower abdomen. Her height is five foot four,
Speaker 1: weight is two hundred pounds BMI thirty four point three.
Speaker 1: A transvaginal ultrasound reveals enlarged ovaries with multiple small follicles
Speaker 1: arranged peripherally. Differentials will rule DOWNT and the patient was
Speaker 1: diagnosed with PCOS. Which of the following is the most
Speaker 1: appropriate first step in managing her infertility? A clomiphene citrate,
Speaker 1: B letrasol, C met foreman D spirrinalactone E lifestyle change
Speaker 1: weight loss, So that is going to be E weight loss.
Speaker 1: So this patient has a BMI of thirty four point three,
Speaker 1: so she is classified as obese and for younger women
Speaker 1: with PCOS and inovulatory infertility, attempts at weight loss should
Speaker 1: be attempted first. In those with obesity. If this does
Speaker 1: not restore ovulatory cycles, ovulation induction is attempted next, usually
Speaker 1: with letrasol. Question three. A twenty five year old woman
Speaker 1: presents to the clinic after noticing increasing facial hair growth
Speaker 1: acne in irregular menstrual cycles over the past year. She
Speaker 1: reports that her periods now occur every two to three months.
Speaker 1: After researching the line, she believes she has polycystic ovary
Speaker 1: syndrome and requests treatment to help regulate her cycles and
Speaker 1: reduce the hair growth. She's otherwise healthy. Not taking any medication,
Speaker 1: denies galactoria, headaches, visual changes, heater, cold intolerance, or fatigue.
Speaker 1: Physical examination confirms hersaitism and reveals no other abnormalities. BMI
Speaker 1: is twenty seven. Which of the following is the most
Speaker 1: appropriate next step in management of this patient. A initiate
Speaker 1: treatment with combined oral contraceptives. B prescribes sphere and lactone
Speaker 1: for hersuitism, C refer for laser hair removal. D conduct
Speaker 1: a diagnostic workup to exclude other causes of hyper androgenism
Speaker 1: and oligomenerrhea. Or E suggests lifestyle changes diet and exercise.
Speaker 1: So the correct answer is D conduct a diagnostic workup
Speaker 1: to exclude other causes of hyper androgenism and oligomenarhea. While
Speaker 1: all of these are decent answers and may all be
Speaker 1: adequate treatment options at some point in the future for
Speaker 1: this patient. The first step before initiating any form of
Speaker 1: treatment for a patient with the expected PACs is the
Speaker 1: first ensured that they have piacos. And while she has
Speaker 1: some convincing symptoms based on the Rotterdam criteria, we can't
Speaker 1: forget that Rotterdam criteria also requires exclusion of other conditions
Speaker 1: that mimic PACs before making the diagnosis. So we need
Speaker 1: to roll out our differentials to ensure we are treating
Speaker 1: the right thing. So start in the apartment for those
Speaker 1: differentials APT, adrenal, pituitary, thyroid, among others. Question four, a
Speaker 1: twenty nine year old woman with PCUS wishes to conceive.
Speaker 1: Over the past six months, she has attempted lifestyle modification,
Speaker 1: including dietary changes, increase physical activity, and has achieved modest
Speaker 1: weight loss. Despite these efforts, he continues to experience and
Speaker 1: ovulatory cycles. According to current evidence, which is the most
Speaker 1: appropriate first line treatment option for ovulation induction for this
Speaker 1: patient A chlomiphene citrate, b letrazol, C met foreman D,
Speaker 1: gonadotropins E laparoscopic ovarian drilling. So the correct answer is
Speaker 1: going to be b letrozol. So remember, let's tresol your
Speaker 1: lettuce ball in Santa's right hand is the first line
Speaker 1: ovulation induction agent over klomaphene citrate Answer A and met
Speaker 1: format Answer C, which are both less effective for live
Speaker 1: birth rates than electrosol and the other two options gonadotropins.
Speaker 1: Exogenous gonadotropin regimens are complex and expensive and considered second line,
Speaker 1: and of course laparoscopic ovarian drilling also referred to as
Speaker 1: ovarian diathermy or electrocoagulation. This is a surgical option, meaning
Speaker 1: more invasive, and would generally only be utilize after the
Speaker 1: patient has tried and failed pharmacotherapy. All right, So that
Speaker 1: was picos. I hope that was helpful. Thank you so
Speaker 1: much for the support of the and best of luck
Speaker 1: in school.