all right good morning everyone so excited to see you all here we're going to get started in just a little bit if you don't mind turning on your chat box saying hello where you are logging in from really grateful you all are here excellent we're going to get started in just a little bit thank you all again for joining all right we have suan from India JY from Michigan great to see everyone we have Amberly from delr Beach Florida Arlette from Augusta Georgia jtil from Arizona excellent Asma from Pakistan wonderful hey iel nice to see you excellent we got a great crowd here today if you're just joining us I'd love for you to open up your chat box say hello where you're logging in from we have over 300 people who have registered for this webinar we're going to get started in just about a minute please note that if you are on social media or you have friends that are actually uh studying for this exam go ahead and invite them I'm actually going to provide you guys the YouTube link you can post it on your Instagram story as you spend this hour with me you can also kindly send it to any of your colleagues who are preparing for this exam Wonderful Paul hello from Portugal sarin from Fresno California Sarah from Michigan excellent and if you're just joining us kindly open up the chat box say hello where you're logging in from this is going to be a great Dynamic session I'm excited for you all to be here with me today if you all don't mind just a quick little audio visual check you all can hear me okay good audio you can see me okay good video and you can see me right on the screen right here is that correct Saron is saying yes Madonna Amberly everybody is saying yes I just want to make sure before we go ahead and get started so it is two minutes past the hour and so I do want to give you all a warm welcome and thank you all for joining on time my name is Rahul deania and I am a practicing pediatric critical care physician I also have my masters in medical education just graduated this past year super excited to share my passion in medical education with you over this next hour and a half or so I have particularly been interested in helping students just like you prepare for and Excel on the USMLE step one and Step 2 CK exams that encompasses all of the high stakes exams everywhere from comp all the way to your shelf exams feel free to get in touch with me I also would love if you can follow and share my Instagram account with those around you right now if you are logging in feel free to share this review session snap a picture of your study workspace tag me I would love to connect with each and every one of you now I do want to highlight what makes high Guru so unique I know that there are so many resources out there but what I think makes huru unique is that my whole resource is all about strategy Active Learning and it's an evidence-based resource I focus on not only small minutia details but of vignette focused learning I also like to integrate across different organ systems and you'll see that today little bit of sprinkle in GI little bit of renal involved in Obstetrics and Gynecology I also will give you test taking approaches to questions my courses are Laden with slides that say high Guru test taking tip so that not only can you get these questions right in the review but when you're sitting down for your fulllength nbmes you know how to tackle various Chief complaints and finally as you can see I'm very energetic and I am very passionate about making sure that not only do you get the content integration and test taking but you are a peak performer on exam day you are happy studying you have the enthusiasm the Curiosity I recognize that dedicated study is not just a physical and a mental grind it's an emotional grind and that's why I focus on test taking psychology as well so whenever I tutor with uh students one on one or work with medical schools I focus on this Triad I focus on hey how do we get good content with clinical reasoning especially as it relates to shelf and step 2 CK how do we make sure that you are optimal every day when you wake up in dedicated study and I leverage powerful tools such as notion to help you you synthesize your nbme and U World notes and plan your whole dedicated study out most importantly and right now the current count is 150 students just in the zoom classroom many on YouTube live but this is my favorite part about hauru we are a global community of lifelong Learners in medicine we have people from the United States all the way to Pakistan and Beyond and this is what makes learning medicine so fun this exam as challenging as it is unites us all what I've also been very to do through my usml courses especially for shelf and step 2 CK I have a course and students here have utiliz this course and as you can see over the past year or so this course has really helped students pass and kickass on the usml Step 2 CK exam and I'm very grateful to work with students one-on-one and have them leverage my course in their preparation and I would love to have you all join if you feel like it is going to be optimal for you as a student I do want to let you all know that I also have some free videos on YouTube that kind of gives you a little bit of a flavor as to how I teach many of you have utilized the nbme step one playlist how many of you all go ahead and put into the chat utilize the nbme top concepts for step one did you all utilize that for step one okay mahare did MOA did keran did awesome very good so I'm building this for step two as well so I'm excited for you to be a part of this journey as well and thank you all for your continued support now I do want to go into how Step 2 CK is different one thing I will say is that step 2 CK truly is a build from Step One and so what I mean by that is that in order for you to be very successful on shelf and step two CK it's important to really be a master at the basic sciences and that's where today we're going to be going through so many different pathophysiology Integrations we're going to be going through many mechanisms of disease you want to understand why the symptomatology is occurring and that's what's going to help you on shelf and step two CK now when it comes to step 2 CK as you know the stems are going to be very different right the stems are going to be what is the likely diagnosis which forces you to activate an illness script related to a certain disease what is a likely idology or risk factor typically ideology is going to be related to an underlying pathophysiologic mechanism or risk factor is going to be what in the patient history contributes to this disease and then finally the notorious what is the next best step in management and I'll give you a little bit of a test taking Pearl here next best step in management could be Diagnostics which are typically Labs or Imaging or it could be Therapeutics which is typically pharmacology or surgery and what you will do is assess the patient stability in your nbme vignette to figure out which way you're going to be going now what I really want you all to focus on if you're preparing for any shelf Step 2 CK maybe you're preparing today for OBGYN shelf you need to understand how to take a symptom within the vignette such as for example seizure which the vignette will state shaking in the bilateral upper and lower extremities plus confusion and understand why that is going on okay seizure it's due to inflammation of the brain or chaotic neuronal activity understanding why the pathophysiology is occurring behind the symptomatology makes you extremely successful when you are embarking on Step 2 CK studing and the reason why is because next best step especially if you're looking at the Therapeutics is going to reverse the pathophysiology so you don't need to utilize this crazy anky deck of esoteric treatments what you need to do is you need to say okay a seizure is going to be chaotic excitatory activity what do I need to do I need to inhibit that activity so now reversing the patho fiz how do you inhibit neuronal activity you're going to give benzo diazines which increase Gaba you're going to block fast sodium channels or calcium channels which are going to block Action potentials and thus chaotic neuronal activity what's another thing you could do as a next best step in management well I need to see the seizure pattern throw on an EEG get some head Imaging to see whether or not there's a fosi for the seizures so now you're recognizing that it's not about memorizing different treatments it's about understanding the pathophysiology and just like a UNO card has reversed you're going to be thinking of Therapeutics especially as reversing the underlying pathopysiology so before we do get started today I'm going to give you all a few disclaimers number one what I want you all to do today is stay very active and engaged with me I don't want to be a background noise I want you all to have the same amount of focus with me over the next hour and a half that you will when you're in your Prometric exam day remember when you're in that block three or block four you're going to need optimal focus and today what I will tell you is it is content and question review at the same time think of me today as merging your videos and Ani with high yield question Banks like you world and we're going to put it into one solid review today what I also would encourage you to do to stay active is take out a little piece of paper and jot down some test taking Frameworks or open up a Word document but make sure that you're cutting out distractions take your phone throw it to the side make sure that it's just you your beverage of choice and your notes document because these concepts are going to be extremely high yield they are going to be the way for you to do well on your OBGYN questions so with that I do want to highlight a little bit about how I think about Step 2 CK and this is going to be seen in my courses as well and what you notice here is that let's say we're dealing with endometrial hyperplasia now endometrial hyperplasia typically on the USMLE is going to present with postmenopausal bleeding now endometrial hyperplasia has a pathopysiology and understanding the pathopysiology will allow for you to extrapolate the management so the pathopysiology here is that you have some form of unopposed estrogen maybe in the vignette they put BMI greater than 30 indicating that there is obesity which can peripherally aromatize your androgens and thus increase the amount of estrone and the increased estrone can lead to endometrial hyperplasia it proliferates the endometrial tissue and if that occurs over a long period of time you could get not only breakthrough post-menopausal bleeding but you could get dysplasia and subsequent carcinoma remember chapters one of pathoma cell injury death and adaptations this is the hyperplasia dysplasia and carcinoma sequence so whenever you see this type of History physical in Labs you want to trigger this pathophysiology and say oh what's the next best step in management in a postmenopausal woman and not only are you going to get an ultrasound but hey you might get endometrial biopsy because that takes a quick picture of the endometrial hyperplasia you may want to reduce the unopposed estrogen that is going to be seen in this patient or monitor for any sort of displasia or Nuclear atypia So when we're thinking about postmenopausal bleeding the first very important concept that we're going to be talking about is endometrial hyperplasia now what are the risk factors in general the framework is going to be unopposed estrogen that's extremely high yield for you to know now with unopposed estrogen you can be thinking about obesity because testosterone gets peripherally aromatized to estrone you could be thinking about PCOS remember patients with PCOS may have a overweight or obese Stigmata in your vignette and they have an ovulatory cycles and if they have anovulatory Cycles they have a Persistence of estrogen and with without ovulation they don't make the Corpus ludum and thus they do not have progesterone granulosa cell tumors remember granulosa cells from Step One are going to secrete estrogen if there is a tumor secreting estrogen that can give you un opposeed estrogen and the early men late men early men sees late menopause and that means that you are just going to be exposed to cycles of estrogen over and over and over again now with postmenopausal bleeding what is the next best step in management go ahead and type into the chat box what is the next best step in management and we have over 200 people here this is absolutely phenomenal excellent many of you all are saying endometrial biopsy and if you don't mind changing your chat box to everyone that will be very helpful so then we can all participate together and if you're saying endometrial biopsy you're absolutely correct you may even get a transvaginal ultrasound to see the endometrial thickness or the stripe thickness and that will also be extremely important in your management framework going from least invasive to most invasive and if you have a stripe that is greater than 4 millimeters you may want to consider endometrial biopsy now let's say that the endometrial biopsy shows nuclear atypia and highgrade tumor or high-grade neoplasia what is the next best step well in this situation if the patient is postmenopausal and is not going to be considering any fertility risk benefit ratio then you would proceed with hysterectomy especially when you're seeing signs of neoplasia occurring all right so now let's take one step back and we have a patient with postmenopausal bleeding on your USMLE and the ultrasound shows a localized growth within the wall of the uterus that then extends in a pedunculated fashion into the uterine cavity the extension of a uterine tissue as a pedunculated mass is going to be very characteristic of endometrial pop a lioma or a fibroid could be a differential especially if it was an intramural fibroid but if it was a pedunculated type of tissue that is going to be very characteristic of endometrium power all right so so far are you all enjoying this review yes no maybe so go ahead and type it into the chat all right well what we're going to be doing today guys is we're going to be covering these topics now I'll give you a little bit of a lens on how did I create this review well what I first did was I went through all of the clinical Mastery series forms the nbme Shelf forms and I looked at the topics that are frequently assessed more than three times then I looked into my U World notes and I figured out hey where is there an overlap where nbme and uor are testing multiple times over and over and over and over again and this was the list of topics that I came up with this is the list of topics that I would encourage you to take a snapshot of become masters of this list topics and we are going to review them step by step today over the next hour so are you guys ready to get started yes everybody good all right wonderful I like to have some energy because I know that lectures these days can really be a drag and so my hope is that with all of these questions we will be able to go through things in a systematic way all right we're going to just pause for 30 seconds I'm going to just change my blinds because they're in my eye and I'll be right back all right can everybody see me okay good all right let's go ahead and get started I do want to give you all a quick little uh guidance point and tell you that the full OBGYN review this is uh eight hours of content this is all of the content including the mapped question IDs they are available in my comprehensive usla Step 2 CK course I'm going to just link it right here it is going to be the first link on your right hand side when you open up this web page H guru.com but if you have not yet enrolled and you're enjoying the question-based integrated content and you want to apply it directly and have just some structure as you're going through your shelf exams your rotations as well as Step 2 CK please make sure to enroll in this course all right we're first going to start with obstetrics and this is going to be starting with this question right here a 26-year old woman presents to the emergency department with sudden onset severe abdominal pain and fainting her last menstral period was six weeks ago Vital Signs show a pulse of 110 so she's tartic and a blood pressure of 90 over 50 so she's hypotensive abdominal examination reveals mild distension with diffus tenderness guarding and rebound transvaginal ultrasonography shows no intrauterine pregnancy what is going to be the next best step in management go ahead and type into the chat are you going to get a CT scan hysterosalpingography C hysteroscopy D laparoscopy or E MRI of the pelvis what do you think is the best answer here excellent and if you are saying D laparoscopy you're absolutely correct remember that whenever you see hypotension and tacac cardia you should be thinking shock and in the setting of your OBGYN shelves you may be thinking of hypovolemic or hemorragic shock now what we're noticing here is that this patient may have a ruptured ectopic pregnancy and that's why you have the perianal signs and that is high yield for you to know so in an ectopic pregnancy nbme vignettes usually say that there is an ultrasound that shows pregnancy in the corneum of the uterus or in the parametrium I.E surrounding the endometrium remember that the most common cause or location of a ectopic pregnancy or extra uterine pregnancy is going to be in the ampula of the fallopian tube and that's extremely high yield for you to know now when you're suspecting ectopic pregnancy they'll say that the female had a period about four weeks ago and now comes in with abdominal pain maybe some vaginal bleeding look at the vital signs if the patient is going to be stable what you're going to be doing is you'll get a beta atg and a transvaginal ultrasound remember that ultrasound around five weeks of pregnancy is going to show an intra uterine pregnancy now in ectopic pregnancy you don't see that intrauterine pregnancy and as a result what you're going to be saying is hey now that the pregnancy is not seen in the uterus I need to if the patient is stable deal with that extra uterine pregnancy I need to deal with that ectopic pregnancy now in some cases if the beta HCG is low and there is no fetal cardiac activity then you can use methot remember that Methotrexate is a dihydrofolate reductase inhibitor and that is going to inhibit the DNA of the ectopic pregnancy and thus take care of the ectopic pregnancy or treat the ectopic pregnancy but there are some contraindications things like thrombocytopenia for example or underlying cancer that could be a contraindication for Methotrexate now in this question the patient was unstable and if the patient is UN stap you don't have time to get Diagnostics you don't have time to really um make uh uh medications the first line in therapy what you want to do there is you want to go for laparoscopy because you want to take care of the ruptured ectopic pregnancy and remove it so in the social history in ectopic pregnancy vignettes you may see that the patient has a history of pelvic inflammatory disease the US loves for you to know that P can cause two scarring and that's an extremely high yield mechanism that can then predispose you to getting an ectopic pregnancy in the ampula of the fallopian tube and IUD can also be a risk factor for an ectopic pregnancy and then finally the risk factor could be endometriosis because remember if you have atopic endometrial tissue that is going to be ripe for fertilization to occur at that ectopic endometrial tissue and as a result endometriosis is a risk factor for ectopic pregnancy so one of the test taking tips that I want to give you that can help you throughout usla Step 2 CK preparation is that if you have any menstrating age group female any menstrating age group female who presents with abdominal pain think about beta HCG as the next best step in management remember that you want to get a screening beta HCG in any female who is in that menstrating age that presents with truly any Chief complaint but especially abdominal pain all right let's go ahead and go through this next question a 17-year-old G1 P0 returns for followup four weeks after a dilation and curage or a DNC for a spontaneous abortion at 13 weeks dation she reports no bleeding or pain her initial beta HG was greater than 50,000 before the dilation and curage serial beta HCG levels poost DNC have plateaued and actually have slightly increased to greater than 14,000 which of the following do we think is the likely diagnosis a endometritis b gestational trophoblastic neoplasia C hia tior mole D retain products of conception or e septic abortion what do you think is the best answer here wonderful if you are going to be saying the gestational trophoblastic disease I apologize for the momer you're absolutely correct remember that if a patient is going to be post DNC and they went in with greater than 50,000 on their um on their uh uh beta HCG levels you are going to be thinking of a molar pregnancy a molar pregnancy remember is going to be an abnormal pregnancy and after DNC if you do not see the beta HCG going down then you're worried about gational troph blastic neoplasia I.E you are worried that there is going to be a neoplastic proliferation of that trophoblastic tissue and so the best answer here is going to be B and again the whole concept here is that you have to follow beta HCG levels as they go down especially when you are going to be worried about a molar pregnancy or even frankly an ectopic pregnancy serial beta HG monitoring is going to be key remember that the patient may have had a molar pregnancy going in post n c the patient ended up then getting rid of some of that tissue and it could have now malignantly uh transformed and that's why B gestational trophop plastic neoplasia is the best answer so what we're going to be talking about is hyap for mole now the molar pregnancy remember is going to be when a sperm is going to go into an empty ovam and then duplicate and that's called a complete mole you can say completely dad's fault or when there is an ovom that is going to be fertilized with two sperm again molar pregnancies are abnormal pregnancies and it is going to be an abnormal proliferation of the ciso and cytotrophoblast now remember that the nbme vignette features are going to be the following so what do they put in the nbme vignette they say number one first trimester bleeding whenever you see first trimester bleeding and a Skyrocket beta HCG you should be thinking about molar pregnancy and that's extremely high yield for you to know another thing that they will say is that the gestational age and the uterine size are going to be very discrepant they'll say that the uterine size is at the umbilicus indicating that maybe the pregnancy is at 20 weeks because between 20 and 22 weeks that's when the pregnancy is going to be right at the umbilicus and they'll say that the patient is actually 16 weeks gestation so whenever there's that discrepancy in that first second trimester you are going to be worried about a hia tior mole other thing that we've talked about is going to be the elevated beta HCG and hi tior mole or molar pregnancies can actually present like preamps in the first trimester and so whenever you have a patient that is less than 20 weeks and has signs and symptoms of preclampsia you want to pay your respects to hia to deform mole now remember that ultrasound is going to show that cluster of grapes or snowstorm appearance and what that basically represents is that abnormal tissue that is going to be proliferating proliferating proliferating and that's why you get the uterine size that is going to be greater than the gestational age now what is the acidbase abnormality in patients who present with hyperemesis gravidarum which is going to be another presentation of Hyo tior mole go ahead and type that into the chat what is going to be the acidbase abnormality a little bit of pH integration here excellent if you're saying hypochloremic hypokalemic metabolic alkalosis you're absolutely correct and remember that if you have a very Skyrocket beta HCG that Skyrocket beta HCG can actually induce a lot of nausea and vomiting and as a result when the patient is going to have hyper MSS gravidarum we are going to need to make sure we fluid resuscitate them we could give Pur doxine or H1 antagonist such as doc salamine which is going to be an antia medication another way that digestal trophoblastic disease or h tior mole can present is a theatine cyst and that is just basically because you have excess amount of beta HCG and that can then stimulate the ovarian tissue so TI it to theform Mo remember we talked about the pathophysiology complete and partial we talked about how first trimester bleeding Skyrocket beta HCG increased uterine size that is discrepant from the gestational age we talked about the presentation of hyperemesis gravidarum and theatine cyst what you want to do is you want to take out that molar pregnancy dilation and curage follow the beta atg levels down if they start going up you worry about a malignant transformation so what is going to be this ultrasound finding go ahead and type it into the chat what is this ultrasound finding for ida4 mole excellent if you're saying snowstorm appearance you are absolutely correct and another integration that I want to bring in here is P57 pathological staining now remember that P57 is going to be found on maternal cells so partial moles in which you are going to have the ovam that is going to be fertilized by two sperm because it is Dad and Mom partial mole because Mom's tissue is there you're going to be P57 positive in a partial mole whereas a complete mole is going to be no P57 and so that is how you can also differentiate between partial and complete mole all right so what we're going to be doing now is we are going to be focusing on first trimester abdominal pain remember first trimester leading you should be thinking about a few things you should be thinking about hey maybe is this an ectopic pregnancy first trimester bleeding it could even be a abortion first trimester bleeding you could be thinking about molar pregnancy what if the patient comes in with just first trimester abdominal pain what are some of the key Frameworks that nbme are going to assess you on number one you have to be thinking of gynecological causes you have to be thinking second of urinary causes and number three of gastrointestinal causes so we're going to go through each one of this let's say that the US MLA said unilateral ad nexal tenderness positive beta HCG and no intrauterine pregnancy that is going to be your ectopic pregnancy what if the US MLA said first trimester abdominal pain and then you have positive beta HCG you are less than 20 weeks you have have vaginal bleeding and an intrauterine pregnancy what is the diagnosis here go ahead and type it into the chat good excellent some sort of abortion and there are different types and we're going to be covering those different types what if the ud USMLE said you have a negative beta atg with your first trimester abdominal pain but you have adal tenderness and decrease Doppler on transvaginal ultrasound what do you think is going to be the likely diagnosis here yes if you're saying ovarian torsion you are correct so make sure to pause this video if you're watching it at another time and go through each of the key vignette features for gynecologic causes of first trimester bleeding or an abdominal pain excuse me now urinary causes what if they gave you disuria urgency and a urine analysis that shows a positive nitrite and Luc estr that is going to be very characteristic of just acute cystitis remember that if they are going to put plus CVA tenderness you could be thinking of pylon nephritis and pylon nephritis needs systemic antibiotic therapy what if they put nausea flank pain and a UA showing rbcs microscopic hematuria you could be thinking that the first trimester abdominal pain is due to renal stone or nephrolithiasis what if they put on your usale nausea vomiting fever and right lower quadrant tenderness and they gave you Labs that showed lucos cytosis that is going to be appendicitis and I just also want to let you know that let's say that the patient is in the third trimester and they have nausea vomiting fever and abdominal pain what the nbme likes for you to know is that sometimes because the patient has a gravid uterus in a pregnancy you could get appendicitis that can actually be in the right upper quadrant or abdominal pain in the right upper quadrant just because the anatomy is distorted with that gravid uterus and I just want to really emphasize that high yield physical exam finding so what we're going to be doing is we're going to be breaking down first trimester abdominal pain in a little bit more detail I'm going to focus on the gynecological causes and what we're going to be focused on is this vignette right here where you have a positive beta HCG the patient is less than 20 weeks and has an intrauterine pregnancy but not only does the patient have abdominal pain but they also have in the vignette they have vaginal bleeding this is where you're going to be thinking about your abortion and I am going to give you a very simple pneumonic or a simple trick to help you keep the abortion straight the first thing that I want you guys to say is I is open to the cervix my eye is open to the cervix so in your vignettes on the physical exam if you see first trimester bleeding and an open cervix It could only be inevitable or incomplete and how do you tell the difference well remember in incomplete there is incomplete Passage of conceptual project products in incomplete they will say they passed some tissue or a partial fetus is seen remember that threatened and complete abortions do not start with i and so the cervix is going to be closed in a complete abortion the patient has a history of passing significant tissue and cloths and that's where they'll say that the uterus is empty because the patient just passed all of the products of conception in a threatened abortion you are going to see the cervical o close but there could be a bulge of the fetal Sac that is going to be there plus the vaginal bleeding I.E there is no products of conception exposed in a threatened abortion and now what about Mist abortion in Mist abortion the cervix is closed because it doesn't start with i and what they'll say is that there's no fetal cardiac activity fetal cardiac activity is absent and the pneumonic that I like to say is I miss the baby I miss the baby so there's no fetal cardiac activity so this is a very nice integrated slide and I wanted to focus on making the delineation between first trimester bleeding and third trimester bleeding remember first trimester bleeding what were your open cervix abortions that is your inevitable and you're incomplete in the inevitable you are going to see that bulge and the cervix is going to be open in incomplete you're going to get incomplete passage of products the closed cervix first trimester bleeding pathologies are going to be threatened in which you do have fetal cardiac activity missed in which you don't have fetal cardiac activity and complete which the cervix is closed and all of the parts were exposed so they may say ultrasound shows an empty uterus third trimester bleeding I worry about placental abnormalities because the baby and the placenta are welldeveloped so placental abnormalities you worry about placenta previa as well as placental abruption how do you tell the difference well with Previa it is painless third trimester bleeding with abruption it is painful third trimester bleeding Vasa Privia is going to be also painless bleeding but that is going to be after rupture of membranes and that's because in the actual amniotic sac the blood vessels of the umbilical cord were abnormally implanted so once you have rupture of membranes the patient can actually have instability the fetal tracing may show Category 3 and you will get that third trimester bleeding with Vasa preia there's also going to be placenta ACR now placenta ACR is going to be a patient on your nbme that is going to have first off recurrent dnc's and why they bring that up either recurrent dnc's or C-sections is because you basically agitated the endometrium and the myometrium as a result in this pregnancy what's going to be challenging to deliver is the placenta so a prolonged third stage of Labor which is the delivery of the placenta is the first characteristic of placenta ACR as well as significant postpartum hemorr and again placenta ACR is when the placental tissue goes into the myometrium what is it called when endometrial tissue goes into the myometrium go ahead and type that into the chat what is it called when endometrial tissue goes into the myometrium and if you're saying ad no meiosis you are absolutely correct remember that if you have placental abruption you could even have disseminated intravascular coagulation let's do a quick Arrow question with DIC you get low platelets high PT I PT and a low fibrinogen these are all going to be the key lab characteristics of disseminated intravascular coagulation and that is seen in placental abruption as well as with retained products of conception all right so let's go ahead and go into this vignette a 35-year-old woman at 6 weeks gestation presents with vaginal bleeding her initial beta HCG is 450 and ultrasound shows a thickened endometrial stripe with no Fe ho one week later her beta HCG has decreased to 90 what is the next best step in management so we have a patient who is now a downtrending beta HCG no fetal pole that is seen and the next best step actually is going to continue to monitor the beta HG because again the patient is going to be stable and if the patient is stable and the patient agrees as we're seeing a downtrend one more measurement of beta HCG you want to in these spontaneous abortions you want to make sure that we go down to zero with the beta HCG with serial monitoring similar to what we talked about with molar pregnancies you want to make sure that there is a downward decline in your beta HCG levels all right so this slide is very high yield and integrated because what we're going to be doing is we're going to create a quick framework for pregnancy and the illness grips are going to be rooted to the weaks that they give you within the usml vignette so remember first trimester we talked about molar pregnancies and the different spontaneous abortions third trimester bleeding you worry about placental pathologies if the patient is in third trimester they may even tell you to interpret the uterine tracings or the fetal uterine tracings which will go through the pneumonic ve chop which talks about variable decelerations early Des cels late D cells Etc now remember that at the 24 we Mark patients are going to get the oral glucose challenge test at 28 weeks mothers are going to get rogam if they are RH negative now remember you not only dose the rogam at 28 weeks but anytime there was fetal mixing let's say that they had a spontaneous abortion and the mom is Rh negative you may have to give the rogam or let's say postpartum there was some sort of fetal mixing you have to give the rogam remember postpartum in a Rh negative mom you are going to send the KB test or the CER bootkey test and that is going to give you a recommendation whether or not you need to redos rogam for the RH negative mother but at 28 weeks you are going to be giving the mother Rogan now another point that I want to bring up is at 34 weeks that's when we're thinking a lot about fetal lung maturity and remember that if the baby is going to be even less than 37 weeks we are going to give mothers beta methasone because maternal steroids actually is going to promote fetal lung maturity beta methasone increases endogenous fetal surfactant production and so whenever you're thinking about even on your ped shelf less than 37 weeks you're going to be worried about fetal lung compromise I.E neonatal respiratory distress syndrome all right so when you're going to be thinking about the 36 week Mark you're going to be thinking about GBS screening and remember that that is going to be a risk factor for neonatal sepsis is if Mom was GBS positive and especially untreated and then also in the third trimester usml questions will be going through preclampsia eclampsia and help which is hemolysis elevated liver enzymes and low platelets so remember preclampsia eclampsia help this is more of third trimester pathologies so why I give this delineation is because you don't want to you know start saying preclampsia in the first trimester you don't want to start saying uh uh doing GBS in the first trimester you want to look at the weeks that's very important in your USM questions now one of the things that we're going to be talking about is hypertension in pregnancy and remember that in pregnancy what we are going to be thinking of is dosing anti-hypertensives whether or not they are going to be before the 20 week Mark or after the 20 week Mark so we're going to go through that in a few slides but what I do want to turn your attention to is what if we had premature labor remember labor is going to be defined as uterine contractions with cervical change and if we have premature labor let's say that the baby is going to be less than 32 weeks to stational age you're going to be considering magnesium tocolytic as well as beta methasone beta methasone for the lung maturity at 32 to 34 weeks you're going to be thinking again of too litics and Beta methasone And if you have premature labor between 34 and 37 weeks you're just going to be considering giving beta methasone so beta methasone is for any premature labor less than 37 weeks now what are the too litics that are going to be employed if there is labor before 34 weeks and that is typically going to be Nettie the pneumonic that I like to use is it's not my time and these are going to be the too litics that are going to be potentially utilized when you have premature labor it's not my time I for endome n for netop p my magnesium time tributal it's not my time and remember I do want to call your attention to endome that then is going to reduce the amount of cyc oinas reduce the amount of prostaglandins and you can get cardiac abnormalities because now you don't have the PDA and that's high yield for you to know typically the tocolytic that is going to be used is going to be netop and neopine again is going to be employed these tocolytics if the baby is going to be coming out less than 34 weeks all right let's go ahead and go through this VI what is the most likely explanation for the findings on the fetal heart tracing a 29-year-old woman G3 P2 at 39 weeks just station is admitted for labor induction due to blood pressure of 155 over 90 she has a history of chronic hypertension managed with meth dopa ultrasound shows fetal growth restriction and 4 hours after starting oxytocin to augment labor the cervix is 6 cm dilated a fetal heart rate tracing is shown so as you can see this is the uterine contraction and we see fetal heart rate decelerations after the uterine contractions so what do you think is going to be the most likely explanation a compensated fetal stress B umbilical cord compression C pressure on the fetal head D uteral placental insufficiency or E normal fetal heart rate what do we think is the best answer here excellent if you are saying D uteroplacental insufficiency you are absolutely correct remember there is a pneumonic feel chop okay so what V chop tells us is that variable decelerations are going to be due to cord compression early decelerations are going to be due to head compression accelerations are going to be normal and L late decelerations which is what we see in this question is going to be due to uteroplacental insufficiency and that is where you are now getting blood flow cut off to the baby now as you note this mother had chronic hypertension and if you have chronic hypertension that is a risk factor for placental hypoperfusion and that's why the baby had fetal growth restriction so when you see late decelerations that's a obstetrical emergency and so there are going to be some management steps that you're going to be considering you're going to stop the augmentation of Labor you're going to give Mom oxygen you may reposition her but if none of those things are going to help or work you're going to consider emergent C-section because what uteroplacental insufficiency means is that you are going to have fetal distress the the blood supply to the baby the actual oxygen delivery to the baby's brain is going to be compromised and that's what late decelerations are going to indicate so I am going to give you a normal fetal heart tracing remember normal fetal heart tracing shows intermittent early or variable decelerations now remember variable decelerations are going to be shaped in a V and they're variable they're not early they're not late I.E they're variably related to the uterine contraction they're going to be less than 30 seconds so that's why it is going to have a vshape so some variable decelerations less than 50% of the tracing is actually okay intermittent early decelerations is okay as well now what we want to be thinking of is the Baseline heart rate of the baby and typically you want the Baseline heart rate of the baby to be anywhere from 100 to 160 and you can even have some variability where there's accelerations decelerations accelerations decelerations that's called variability remember that if you are going to have maternal fever the baby can have a heart rate of like 180 because maternal fever can transit to the baby in terms of that fetal tacac cardia what we also want to note is that if there's minimal variability and everything else looks okay but there's minimal variability the heart rate is still between 110 and 160 maybe the baby is just sleeping and that's a high yield nbme question however when you are seeing bra cardia of the baby that is going to be indicating fetal distress and that's extremely important for you to keep in mind so here is VE chop in action we're going to do a little bit of a space repetition review remember that acceleration is normal fetal oxygenation and it is accelerating around the time of the contraction the heart rate is early decelerations they are going to represent head compression and this is typically because as you have the uterine contraction there is going to be a vagal response that is going to be generated and that head compression can cause you to have that bagel resp respond in that quick little early deceleration variable decelerations there's no real association with the uterine contraction it's variable and it is a vshape and go ahead and type into the chat what does the variable deceleration represent type into the chat what does the variable deceleration represent and I want everybody to answer here excellent if you are saying chord compression you are absolutely correct and remember that I am going here variable cord compression now late deceleration we talked about this in our last question this is typically going to be known as a category 3 concerning finding and it is going to represent uteroplacental insufficiency that's where you have the peak of the contraction and the nadier of the deceleration and remember it's a u shape with late deceleration remember the adequate uterine contractions if you have a intrauterine pressure catheter is going to be greater than 200 Mont Vio units in a strip and that is something that also is frequently assessed and how do you augment that contraction you can give oxytocin to augment the uterine contractions now I have seen nbme questions which focus on what can cause uteroplacental insufficiency well we talked about hypertension can cause it smoking can definitely cause you to have placental hypoperfusion think about smoking as making the blood vessels of the placenta very Twitchy and what else you're going to be thinking about lupus remember that lupus you can get microthrombosis with lupus lupus is a hyper quable State and that micro thrombosis because of very high yield antiphospholipid antibody can cause you to have placental hypoperfusion can also cause you to have recurrent first trimester abortion so if they say hey the baby is or the uh mother is G3 P0 you could be thinking about a diagnosis of Lupus all right let's go ahead and go through this next question I want to just take a pause is everybody learning everything okay I know there there are small nuances here and there but I would encourage you all to really take that big picture approach and what's the big picture approach I need to get baby out of mom safely and these are different things that we need to keep in mind in terms of numbers and nuances but the big picture is I need to safely get a baby out of Mom all right let's go ahead and go into this next vignette given the underlying diagnosis what is the most likely complication during labor here we go a 28-year-old woman G2 P1 at 36 weeks gestation is admitted for evaluation due to worsening headache and swelling in her hands and feet over the last few days she reports also seeing spots in her vision her pregnancy has been otherwise uncomplicated Vital Signs include a blood pressure that is is elevated pulse of 88 and respirations that are fine physical exam reveals bilateral pitting edema again that pitting edema is correlated to the swelling that she has in her hands and feet and laboratory studies are shown so let's go through and break down the labs hemoglobin is fine lucite count is fine platelet count is uh going to be slightly low and we are going to have elevated serum creatinine and urine proteinuria that is going to be seen so given the underlying diagnosis what do you think is the underlying diagnosis first what is the most likely complication during labor a placental vasospasm and eskia B amniotic fluid entering maternal circulation C uterine contractility dysfunction due to edema d m severe maternal systemic inflammatory response or E myometrial rupture due to increased intrauterine pressure what do you think is the best answer here excellent so this is going to be preclampsia with severe features and remember that pre eclampsia is going to be on the Spectrum in the sense that you get placental hypo profusion that's the pathophysiologic theme I'm building in these last few slides and preclampsia can be associated with placental vasospasm and esmia that can then lead to placental abruption and that's where the placenta is going to kind of come off of the uterine lining and so that is high yield for you to know amniotic fluid olism is going to be answer Choice B severe maternal systemic inflammatory response that's going to be Perry partum or uh intrapartum sepsis and this is going to be your uterine rupture and remember uterine rupture the high yield nbme term that they say is loss of fetal station so they'll say oh they were plus two and now they're to minus one or something like that a loss of fetal station all right let's go ahead and go through this nbme vignette what is the most likely diagnosis a 35-year-old woman at 16 weeks dation presents for a follow-up with the blood pressure of 150 over 98 she reports a 10-day history of moderate headaches but no vision changes she has no history of serious illness and her only medication is a prenatal vitamin A BMI is going to be noted at 33 fetal heart rate looks pretty good and there's just Trace proteinuria what is the likely diagnosis a essential hypertension B gestational hypertension c preclampsia d superimposed preclampsia on essential hypertension or E transient hypertension what do you think is the best answer here all right well if you're thinking about this question what we're noticing is that the mom is going to be less than 20 weeks and if you're going to be less than 20 weeks and you have hypertension most likely it is going to be essential hypertention and so I really want you all to focus on the timeline so you take the whole gational Spectrum 20 weeks if you have hypertension before 20 weeks you're going to be thinking of essential or chronic hypertension and remember that even if the patient has some proteinuria at that time maybe it's because they have chronic kidney disease the point being here is that less than 20 weeks you just think about the patient kind of like an internal medicine patient oh they might have chronic kidney disease they may have for example essential hypertension a differential for sure is going to be the molar pregnancy especially if you have discrepant uter size especially if you have hyperemesis gravitum signs of maybe preeclampsia or even vaginal bleeding after 20 weeks if there is hypertension you need to be thinking about gestational hypertension if there's proera or edema of the extremities you're going to be worried about preclampsia and anytime I think of the word preclampsia not only am I triggered by hypertension swelling right upper quadrant pain what I really focus on is severe features means that there's end organ damage so what does that mean is the patient altered does the patient have an elevated creatin you always want to be thinking of end organ damage and help syndrome is kind of on the spectrum of preclampsia eclampsia because again that has end organ damage of the hematologic system of the liver as well so what I want you all to recognize is that when you have arter hypertension there can be spiral artery hypo profusion and as there is spiral artery hypop profusion that can lead you to have endothelial dysfunction and microthrombosis of the placenta and that's why preclampsia for example can be associated with placental abruption because you have Micro thrombosis as there is going to be a high systemic vascular resistance chronic hypertension can cause you to have what can cause you to have fetal growth restriction and that's because again you get placental hypoperfusion so here's this theme that high svr State over a long period of time can lead you to different placental abnormalities so one of the things that I wanted to integrate right here are the agents that we use for hypertension and pregnancy the pneumonic that I like to use is hypertensive moms love netop hypertensive moms love netop and where did we see nyine well we saw nyine in as a calcium channel blocker when we are going to be talking about premature labor so what we're going to be doing is we're going to be integrating the USM step one mechanisms with these different anti-hypertensive agents so hydraline remember is going to increase cylic GMP methyldopa is Alpha 2 Agonist I apologize for that typo LOLOL is going to be a Alpha One blocker and a non-specific beta blocker and because it's a non-specific beta blocker for patients who are predisposed to Bronco constriction such as patients with asthma or if the patient has rer cardia like let's say their heart rate is like around 60 or below you don't want to give labetalol so remember labetalol there are these two high yield contraindications bra cardian asthma and then finally netop is going to be a calcium channel blocker the pneumonic I like to use hypertensive moms love netop you don't use ACE inhibitors in pregnancy because it's a patogen It's associated with fetal uh uh renal dis Genesis so we have talked about preeclampsia and preclampsia here's the illness script a female who has high blood pressure and cenera edema right upper quadrant pain remember preclampsia I've seen an nbme question that preclampsia can even occur after pregnancy and that's also important for us to keep on our differential but when you have third trimester hypertension you to be worried about pre-clamp so I'm now going to give you the various stems that the USM gives you with preclampsia here we go why does the patient have right uper quadrant pain can you guys put into the chat why does the patient have right upper quadrant pain excellent stretching of the gleasons or stretching of the liver capsule with preclampsia what is the next best step in management give magnesium and you can also consider delivery but magnesium for neural protection speaking of magnesium how does magnesium toxicity present go ahead and type that into the chat how does magnesium toxicity present excellent if you are saying respiratory depression or neurological depression such as he Ionia you're absolutely correct another thing that I like to put in here is exacerbation of myasthenia gravis remember myosin gravis is going to be antibodies to the nicotinic Ayo coin receptor if the patient is given magnesium they can actually have a mytina crisis which is going to be categorized characterized by diffuse weakness and so in order to reverse that you give calcium so that then their muscles get stronger what patient population is at increased risk for magnesium toxicity if I keep giving them magnesium ah patients who have renal insufficiency or CKD because remember magnesium is an electrolyte cleared by the kidney what are pulmonary manifestations of pre-clamp with severe features remember that last slide I talked about what end organ damage so end organ damage could be the liver could be the uh CNS but what are the pulmonary manifest inations and that is going to be pulmonary edema remember that in preclampsia you have increased systemic vascular resistance that can be a high afterload state to the LV and that pressure can be transmitted into the pulmonary capillaries by an increase in your pulmonary capillary hydrostatic pressure remember that you have proteinuria and because you have proteinuria you have low oncotic pressure and that can also facilitate pulmonary edema so remember you see preclampsia then think end organs and the end organ representation of pulmonary insufficiency is pulmonary edema what are fetal complications of maternal preeclampsia we've talked about this go ahead and type it into the chat fetal complications of maternal preclampsia excellent if you're saying fetal growth restriction due to uteroplacental insufficiency you're absolutely correct all right how about this one a mother with multiple gestations had preeclampsia in the prior pregnancy what is an important step in management for this pregnancy if a mom has a history of pre eclampsia very good if you said lowd dose aspirin you're absolutely correct so you want to give aspirin between 12 and 28 weeks gestation optimally you want to give it at around 16 weeks or right between that 12 and 16 week Mark why do I say 12 weeks because if you give Asprin before 12 weeks of gestation guess what you can close the PDA and you can get cardiac abnormalities as a result so that's why we don't start the aspirin too early because the heart is still developing you don't want to close the PDA all right we are going on here almost done with obstr tricks and then we will pivot into Gynecology is everybody doing okay all right I want everybody to stay active and engaged throughout all of this again a lot of different questions are Prometric exam day are you gonna lose energy at six block and just be like yeah I don't care anymore no you're not going to zone out here either so let's go ahead and make sure we stay active and engaged in Focus throughout this which of the following is the most likely finding on the peripheral blood smear we have a 34-year old woman at 34 weeks gestation presents with severe fatigue right upper quadrant pain as well as nausea physical exam shows poor so again signs of anemia blood pressure is very elevated Labs show thrombocytopenia and increased as and ALT a peripheral blood smear is ordered what would you see on the peripheral blood sphere go ahead and read through the answer choices and place your answers into the chat box excellent if you are saying that there is hemolysis there is going to be elevated liver enzymes and low platelets this is help and remember help is a microangiopathy and similar to many microangiopathies what are you going to see schistocytes fragments of rbcs caused by shearing in damage microvasculature again I make these answer choices more so like patho fiz mechanisms remember abnormal ribosomal remnants due to defective arthop poesis this is the basophilic stippling you can see that in for example Cito blastic anemia nuclear remnants with rbcs from splenic dysfunction that's your howl Jolly bodies round rbcs lacking Central po due to membrane defects that's your spherocytes and hereditary spherocytosis cells with missing segments due to oxidative damage that's your bite cells for G6PD deficiency so schistocytes associate with help syndrome high yield all right let's go ahead and close out our obstetric review with these final three slides here we go a 29-year-old woman G3 P2 at 39 weeks to station is admitted 10 hours after rupture of membranes she now has a temperature of 39.1 she is tartic and uterine tenderness is present fetal heart rate Baseline because of the maternal fever is high the patient has mild variable deceleration so overall is doing okay what is the most appropriate next step in management and if you are worried about Coro amnionitis again a mom who is going to have uterine tenderness and fever before they deliver you want to remember initiate broadspectrum antibiotics ampicillin and Genty usually are going to be the go-tos you could also add clinda especially if there is going to be a concern for postpartum Coro or endometritis and the mother had a C-section you would be considering adding clinda to the regimen but typically amp and gent to cover for example group be strep leria Etc but the key that the usla wants you to know is that the common organisms for Cho amnionitis they like for you to know it's polymicrobial so it does have a little bit of Anor robes a little bit of GBS Etc so please note that coronitis the common organism the answer is polymicrobial all right same female here and I'm just going to twist the vignette just a little bit a 29-year-old woman G3 P2 at 39 weeks gestation is admitted 10 hours after membrane rupture so she has uh prom fetal tracing is notable for recurrent variable decelerations that do not improve following amnio infusion so what you're noticing here is that you are going to have a lot of cord compression okay again go back to your ve chop pneumonic variable is going to be cord compression on digital cervical exam a palpating or pulsatile structure is felt within the vagina pulsatile structure is felt within the vagina what is the next best step in management so there's a pulsatile mass in the vagina with variable D cells you need to literally stay on the bed and this is the G Anatomy part where you're rolling the bomb so fast because you are worried about umbilical cord prolaps and that's why you were getting a lot of variable decelerations because the baby's head was compressing the cord as seen in this picture and so when you see the cord in your cervical exam you have to just push the cord up and run directly to C-section this is a emergency integration here is to recognize that whenever you lose a lot of fluid and you have Olo hydram Nails which is going to be defined as a low AFI remember AFI less than five oligo AFI greater than 25 poly hydras but if you have less fluid surrounding the baby there's going to be an increased risk for cord compression and aloh hydros remember in the baby is associated with pulmonary hypoplasia remember that the baby needs that amnionic fluid for lung development and so oligohydramnios Potter sequins pulmonary hypoplasia that is going to be tested not only on OB but on peed shelf so that's why I wanted to include it here all right this is going to be our last obgy in slide and what I want to focus on here guys is the mother who has difficulty with breastfeeding so they have delivered congratulations and and now the mother has difficulty in breastfeeding what are going to be some differentials let's go through it let's say that the US MLA put the mom had a complicated delivery with intrapartum hypotension so maybe they said that there was a lot of bleeding so the mom had hemorragic shock and now has difficulty with breastfeeding you worry about shean syndrome absolutely this is going to be eskee of the pituitary and thus you are going to not get the G&R the L H FSH and you're not going to be getting the um uh prolactin in uh particular so remember that the pituitary getting um eskia typically you're not going to get the good LH and FSH as well as prolactin what if they said that there is going to be complicated delivery but the mom had headache visual changes as well as low blood pressure well this is actually going to be pituitary apoplexy this is actually going to be a hemorrhage of that pituitary gland and that can then give you not only difficulty with breastfeeding but guess what it can give you a central adrenal insufficiency and that's why you get the hypotension is because you get a central low act and that's why you get hypotension but again this is esea this is going to be hemorrage so you want to really differentiate it and remember that the headache and visual changes will tell you it's more pituitary apoplexy now what if they put cracked nipple this is going to be acute mastitis remember mastitis you can still feed during mastitis that's a high yield point and number two deox ayin to cover mssa and then finally we have the mother who is going to have a crack nipple but over time they have fever breast tenderness and a tender fluctuant mass that is noted and that is going to be breast abscess and remember abscess is going to be a encased infection so you do have to consider drainage for Source control and with that we're going to Pivot and go into Gynecology how do you guys find the review so far wonderful obstetric is a little bit involved so I want you all to really Center yourself stay active and engage Gynecology is going to be next let's go ahead and go into first a very high yield test taking framework now guys my goal as you know is to not just sit here and read you slides or read you off a first aid or whatnot my goal is actually to help you think like a doctor and so let's go through this whenever I'm thinking of GYN questions I always think about it anatomically Volva vagina cervix uterus Fallopian tubes ovary so I kind of just go up the reproductive track but in order for us to understand what are the pathologies that are tested on step two CK and shelf you want to understand what's the pathophysiology of disease that occurs in these areas and this is gold guys let's go through it at the Volva region you worry about infection you worry about even low hormonal stimulation let's say you have a post-menopausal female and now she has itchiness there and a cigarette thin vulva what are you worried about go ahead and type into the chat cigarette thin vulva because of low hormonal stimulation yep low estrogen and you got it like in sclerosis infection could be HSV of the vulva that numbness tingling vesicular lesion other vulvar pathologies barlin glandis when you're going to have that fluctuate mass at the 4 and 7:00 position so infection and L lack of hormonal stimulation are two key pathophys mechanisms of vulva now what about vagina for vagina you can get infection and this is vaginitis and vaginitis let's go through it it's either BV tronus or Canada that are high yield you can be thinking of trauma to that region or maybe a foreign body remember the retain tampon that can cause toxic shock syndrome at the cervix now you're worried primarily of the vignettes related to HPV so I put neoplastic I also put inflammatory remember PID due to neria gonorrhea or chlamidia and that gives you cervical motion tenderness on your vignettes just to Pivot here what are screening recommendations for HPV it starts at 21 you do it every 3 years and starting at AG 30 you can even consider HPV co-testing and make your intervals like 5 years and remember Co testing are for the highrisk strains 16 and 18 what about at the uterus what are some pathophysiologic mechanisms go ahead and type into the chat what are some pathophysiologic mechanisms at the level of the uterus excellent if you're saying infection you're absolutely correct wonderful hyperplasia endometrial hyperplasia you could be thinking of neoplasia benign neoplasia that can be related to even structural abnormalities what am I going for here Lomas and one of the things that they love for you to know is that whenever you are going to get recurrent dnc's or recurrent bouts of pelvic inflammatory disease you can get scarring and that scarring can lead to infertility and we talked about that kind of in our ectopic pregnancy discuss where if you have tubal scarring you could get infertility or ectopic pregnancy as well so speaking of the fallopian tube the paiz mechanisms are infection and then subsequent scarring remember that you could even have a hydro salins in which you have a Fallopian 2be pathology and they say a dilated fallopian tube and that is again due to potentially even an old ectopic pregnancy that was removed so abnormal implantation and tubal scarring are two key mechanisms of disease at the fallopian tube now ovarian pathologies on the USMLE typically patients are going to present especially with neoplasia are going to be presenting with early satiety they may even have increased abdominal circumference because they are going to have the momental caking you also worry about cysts in the ovaries and those cysts can become very heavy heavy similar to tumors of the ovary and that can cause you to have sudden abdominal pain and you worry about torsion so again this gives you a really good framework and your goal is to Now map vignettes underneath this framework okay all right I hope that this was helpful let's go ahead and go into one of the high yield ovarian pathologies and that's PCOS now the pathophysiology of PCOS what you want to note is that PC is associated with insulin resistance in the vignettes the patients are not only going to have the heru ism but pay attention to the BMI and they can even have physical exam findings of hyperinsulinism such as acanthosis nigran but what happens in PCOS is you get an abnormally High LH to FSH ratio and because the androgens are going to be elevated due to the excess LH those androgens can actually not only cause you to have heroism but then with the increased atpo cells that these patients have the androgens can even get peripherally converted to estrone and that then shuts down the FSH and so you do not get follicle maturation because the FSH is going to be low and as a result because you have low FSH due to the peripherally aromatized estrone that is shutting it down you won't get ovulation and that's why PCOS is a risk factor for endometrial hyperplasia and that's because of the increased amounts of estrone and an ovulatory Cycles what is important for us to know is that these patients are going to have lot of cysts on their pelvic ultrasounds that's the Roder Dam criteria they're going to have an ovulation and that manifest as the cysts the high LH gives you the hutis and again the high estone coupled with the anovulation can lead you down the hyperplasia dysplasia carcinoma sequence so the first step in management lifestyle modification for hyper testosterone States you could use finasteride or spirono lactone particularly they love spironolactone because spironolactone is going to be anti-androgenic and that's high yield for you to know oral contraceptives can help in some of these cases and if the patient would like to have a baby because they have an ovulation you need an ovulation stimulatory type of compound and that's why clopine which is a serm that messes up with negative feedback and gives you that ovulation can be used if patients are Desiring fertility another high yield thing for us to know is metformin is going to be used in these patients with their insulin resistance so really want to link PCOS and insulin resistance together as well as these other pathophysiologic principles so what are other causes of anovulation remember that if you have an immature hypothalamic ovarian axis you can have an ovulation I see this as a pediatric intensivist a female just starting period and is having breakthrough bleeding and irregular Cycles pushing syndrome hypercortisolism can cause you to have an ovulation and even hypothyroidism can cause you to have anovulation and you know it could be due to the fact that when you have hypothyroidism you can get Upstream elevated TR and that elevated TR can actually stimulate prolactin and that can mess your whole LH FSH Downstream we're going to move into the vagina now so here are signs of vaginitis and let's say I say that the vignette put recent antibiotic Administration and epithelial cells studded with pleomorphic rods what is that cause of vaginitis and these epithelial cells studded with these pleomorphic rods you're worried about Gardella vaginalis this is Alo known as bacterial vaginosis and they love for you to know the treatment which is flagel or metronidazol what if they say itchy arthemius vagina plus thick white discharge treatment here so thick white discharge you're worried about Canada and so treatment typically is going to be oral fluconazol and high yield for you to know the Moa of all medications but in particular fluconazol remember fluconazol is going to inhibit for 14 Alpha demethylase and as it does that you decrease the fungal cell membrane I.E you decrease the fungal orgol which is part of the fungal cell membrane what if I put yellow green discharge what is wet Mount going to show vaginitis plus yellow green discharge you're going to be seeing felated protozoa and that's characteristic of tricomoniasis do you see how these are two-step thinking questions what if I see vaginitis and then physical exam noting arthemius cervix with punctate hemorrhages what is the likely pharmacological therapy go ahead and type that into the chat excellent and I'm seeing metronidazol but guess what if you are going to have those punctate hemorrhages that is tricomoniasis and remember for tronis you have to treat the patient and the partner and that is high yield in USM question so I put that here for you so tronus yellow green discharge it's hella inflammatory so you have a arthemius cervix with punctate hemorrhages all right last question for vaginitis which vaginitis on wet Mount has preserved normal low vaginal pH 3.8 to 4.5 and that is going to be Canada all the other ones have an elevated vaginal pH Canada is the one that preserves the normal vaginal pH you got it guys all right well we have only four more slides left and I will tell you the last 10 questions on block eight of Step 2 CK you ain't G to stop you're G to keep going let's go ahead and finish off this review strong with this multiple choice question a 37-year-old woman reports one-year history of worsening menstrual pain her periods are regular she had a laparoscopic tubal ligation two years ago so they ligated her Fallopian tubes no abnormalities were found there but now you notice a pelvic exam reveals a soft tender uterus and it is enlarged to about eight we size so en llarge uterus with irregular menstrual pain there are no adal masses which are the following mechanisms best describes this patient's symptoms a ectopic implantation within the fallopian tube B endometrial gland Invasion into the myometrium C ectopic endometrial tissue and nodularity in the culdesac D fallopian tube dilation from chronic obstruction or e in intramural benign soft tissue tumor what do you think is the best answer here so a globular 8we size uterus with menstrual pain chronically you got it if you're thinking about adom myosis you are absolutely correct remember adenomyosis is endometrial gland Invasion into the myometrium ectopic pregnancy is going to be answer Choice a ectopic endometrial tissue and nodularity in the culdesac that is endometriosis and remember endometriosis in the posterior culdesac and in the uterosacral ligaments is going to give you nodularity but it's not going to make your big uterus that you see in this vignette this is going to be hydro cinks and then this is going to be a fibroid and so what we see is a soft tender uterus that is enlarged with worsting menstrual pain adom myosis so what I'm going to do is I'm going to compare and contrast fibroid and adenomiosis two of them both of them excuse me are causes of pelvic pain but there are subtle differences adom myosis it is endometrial invasion of the endometrial tissue into the myometrium you will get a diffusely boggy and diffusely tender uterus these patients can have meta and the management is going to be control their cycles and Nets definitive management for adenomiosis if the patient doesn't desire fertility is going to be hysterctomy if the pain is refractory Now lioma is it going to be a smooth muscle tumor of the myometrium and on ultrasound you'll see the intramural World masses you're going to see not a diffusely large but a very nodular uterus you may even see menaga and that's why menia plus pelvic pain you have to be thinking of these ideologies and management is going to be to shrink the fibroid so very invasive is myomectomy but you can first start with ocps you can start with lupride to just shut down the estrogen production you can even give iuds to just again reduce the hormonal stimulation of these fibroids so what placental pathology has similar pathopysiology to adenomiosis go ahead and type it into the chat what placental pathology has kind of similar pathopysiology to adenomiosis yeah and if you said placenta ACR you're absolutely correct placenta ACR placental tissue into the myometrium adom myosis endometrial tissue into the myometrium think about it anatomically we also want to cover in GYN endometriosis now endometriosis here's the general illness script in you world questions chronic cyclical pelvic pain disparia which is pain with sex and dis Mena in a female it's a chronic Tempo it comes and goes and you notice these qualifiers first line therapy you're going to be thinking of ocps and Nets again you want to regulate for these fibroids adomos all that regulate the cycles and reduce the amount of prostate GL bons that's such a good important point is that even when patients have primary disys Mena that female who misses work because she has very painful periods prostaglandin therap prostaglandin inhibition IE viia nids is going to help because excess prostag glandon are what causing the pain what are the physical exam findings in endometriosis well it depends on where the endometrial tissue is abnormally implanted it could be causing you to have lateral cervical displacement because maybe there's a mass effect going on there could be nodularity of this posterior culdesac where the uterosacral ligaments are so you'll feel the nodularity of that ectopic endometrial tissue you may even get cervical motion tenderness but how do you tell the difference between cervical motion tenderness of PID and cervical motion tenderness of endometriosis well PID the tempo is acute PID there's fever you may even get ovarian engorgement and that's the chocolate ovary or you may get a fixed retroverted uterus because if there are a lot of adhesions and endometriosis here the uterus is going to flip backwards towards the rectum what is the mechanism if there was pain with defecation maybe you have some implantation of endometrial tissue right at the pouch of Douglas so if they have dyschesia you should be worried about endometriosis there and then let's say for example the patient is started on nids and ocps and now continues to have pain this is where you set them up for laparoscopy and you can take out some of those ectopic endometrial tissue with the LA oscopy so it's kind of Diagnostic and therapeutic and with that ladies and gentlemen we are going to end but I want you guys to stick around for just two more minutes this was a long review and you guys did absolutely awesome and I have a great surprise for you all in the chat box what I'm going to be putting here is just some bonus content my wife is a newly minted just graduated residency she's OBGYN and guess what we yesterday teamed up and she did such a phenomenal job to record this bonus content for you go ahead and click this link it covers normal labor I hope you enjoyed this bonus content again my goal is to be very high yield and you will enjoy this quick little chalk talk it's going to push you to review normal labor so please make sure to check this out again if you have not already I'm going to give you just the direct link for the Step 2 CK course please if you have not already signed up for the Step 2 CK course many of you can already attest I see many people already in the course but this allows for you to not only get all the OBGYN content but all the shelf content surgery Pediatrics Internal Medicine test taking Frameworks please please please go ahead and take a look at this and if you have a friend who is going to be also preparing for step one I have a step one course that is going to be in the description as well as I'm going to link it 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