Pathoma Female Genital System and Gestational Pathology Flashcards
What is a Bartholin cyst? What is the analogous structure in males?
Cystic dilation of Bartholin gland (greater vestibular gland) which lubricates the vagina, at the lower vestibule adjacent to vaginal canal
-> Greater vestibular gland is analogous to bulbourethral gland in males
Who tends to get a Bartholin cyst / how does it happen? Is it unilateral or bilateral?
Happens when the duct gets clogged due to infection / STI (usually women of reproductive age)
-> often unilateral
How do we subclassify HPV viruses?
Via DNA sequencing -> there is no difference in antigens.
What is chronic atrophic dermatitis also called and who tends to get it?
Lichen sclerosis (et atrophicus) -> commonly seen in postmenopausal women, with possible autoimmune etiology
What does Lichen sclerosis (LS) look / feel like?
Presents as a white patch (leukoplakia) in a butterfly distribution (symmetric)
-> skin surrounding vulva will be “parchment-like” -> very thin
What are the histologic features of lichen sclerosis?
Thinning of the epidermis - Atrophy of epidermis with absence of epidermal ridges
Fibrosis of the dermis - Replacement of underlying dermis with dense fibrotic collagenous connective tissue
What is the primary worry with lichen sclerosis?
Development of carcinoma of vulva
- > longstanding diseases can progress to non-HPV related vulvar carcinoma related to a p53 mutation
- > generally occurs in elderly women (70s, vs 40s-50s of HPV-related vulvar carcinoma)
How does Lichen Simplex Chronicus (LSC) develop?
Occurs due to chronic rubbing / scratching of skin
-> often seen in patients with chronic, pruritic skin disease like atopic dermatitis, or systemic pruritis (end stage renal disease or liver disease (jaundice))
How does the histology of lichen simplex chronicus differ from lichen sclerosis?
Both present as leukoplakia
Simplex Chronicus - THICKENING of epidermis (often causing leathery vulvar skin, almost like acanthosis nigricans)
Sclerosis - THINNING of epidermis
What must you differentiate from LSC / LS?
Vulvar carcinoma - also presents as leukoplakia
- need to biopsy to definitively tell the difference
What is extramammary Paget disease and how does it present grossly / microscopically?
Malignant epidermal cells in the epidermis of the vulva (skin around vagina)
Presents an an erythematous, pruritic, ulcerated lesion around vulva
Microscopically - large clear tumor cells in epidermis
How is extramammary Paget disease told apart from melanoma (which can sometimes occur on vulva)?
Extramammary Paget disease: PAS+ (stains positive for mucin = carcinoma)
Keratin +, S100-
Melanoma: PAS-, keratin-, S100+ (marker for neural crest derivation)
What structures develop the vaginal epithelium?
Upper 2/3 - From Mullerian duct - columnar epithelium
Lower 1/3 - from Urogenital sinus - SSNK epithelium
-> during development SSNK should come to replace upper 2/3 of vaginal epithelium
What occurs if you are exposed to Diethylstilbestrol in utero and what is the feared complication?
Adenosis - focal persistence of columnar epithelium in the upper vagina
Complication - Clear cell adenocarcinoma
What other complication can occur to daughters exposed to DES in utero? What is DES btw?
Smooth muscle formation abnormalities -> abnormal Mullerian structure development
DES - synthetic estrogen compound -> also increases Mom’s risk for breast cancer
What is the most common childhood malignant soft tissue sarcoma? Where does it usually arise and what is it called if it does?
Rhabdomyosarcoma
Arises as a polypoid, grape-like mass in hollow, mucosa-lined cavities, i.e.:
Nasopharynx
Urinary bladder
Vagina - classic presentation
Called sarcoma botryoides
Oddly enough these are all areas where skeletal muscle is not normally present
What will the cells look like in sarcoma botryoides and how can they be identified?
This tumor is specifically an embryonal rhabdomyosarcoma. The cell type is “rhadomyoblast”
Immature skeletal muscle cells with eccentric nulcei. They will have a cross-striation pattern on histology and will stain positive for actin, myosin, myogenin, and desmin.
What is desmin vs vimentin?
DesMin - intermediate filament of Muscle cells
ViMEntin - MEsenchymal tumors
How does the treatment of CIN and invasive carcinoma differ and why?
CIN - oftentimes very conservative management with followup Pap smear, or cryosurgery / lazer therapy, or removal of the small area.
This is because CIN is still reversible (though less likely from CIN-1 to CIN-3)
Invasive carcinoma - aggressive management -> hysterectomy and lymph node dissection with radiation therapy.
This is because invasive carcinoma is IRREVERSIBLE.
What are the risk factors for CIN?
- Smoking! Important one (along with pancreatic being a counterintuitive one that smoking causes)
- Immunodeficiency -> squamous cell carcinoma of anus or cervix is actually an AIDS-defining illness (CD4 < 500)
Immunodeficiency increases your risk for persistent infection
What is the classically presentation for cervical carcinoma?
Bleeding / post-coital bleeding
What is an extremely common cause of death in cervical carcinoma?
Hydronephrosis with postrenal failure -> due to advanced tumors invading thru anterior uterine wall into bladder, blocking ureters.
What is the confirmatory test for diagnosis of cervical cancer?
Colposcopy - use microscope to examine cervix, then apply acid to identify areas of dysplasia
Biopsy areas of dysplasia -> determine if there is cancer
What are two weaknesses of the Pap smear?
- Not as good for adenocarcinoma - incidence has not gone down
- Invalid if sampling is not done properly at the transformation zone
Do you still need to get Pap smears after HPV vaccination?
Yes -> other nonvaccinated subtypes can still cause CIN
What is the most common cause of dysfunctional uterine bleeding? Who tends to get it?
Anovulatory cycle
-> lack of ovulation occurs, so there is excessive estrogen stimulation of proliferative phase, leading to unscheduled breakdown of stroma
Common at menarche and in perimenopausal women (ovulation never occurred, so no secretory phase)
What causes acute endometritis?
Bacterial infection due to retained products of conception after delivery, miscarriage, abortion, or with a foreign body.
-> i.e. a piece of placenta or instrumentation
Purulent bloody discharge with many PMNs
What is the hallmark of chronic endometritis and what are some common causes?
PLASMA CELLS in the stroma as part of chronic inflammation, as lymphocytes and macrophages are often present in endometrial stroma
Causes: Pelvic inflammatory disease Retained gestational products IUDs -> A. israelii TB -> will show granulomatous inflammation
What is the clinical presentation of endometrial polyps and what are they associated with?
Painless abnormal uterine bleeding
Associated with the use of tamoxifen for breast cancer (endometrial estrogen agonist causes overgrowth)
What is the definition of endometriosis and the most common spot for it? Does the myometrium count?
Endometrial tissue, including both stroma and glands, outside the uterus
Most common spot is the ovary
->involvement of the myometrium is called adenomyosis, and does NOT count as a form of endometriosis, but still presents as PAINFUL uterine bleeding
What are the theories of pathogenesis of endometriosis and how does this relate to endometriosis being found in the following locations: Ovarian cavity Abdominal cavity Abdominal scars Lungs Lymph Nodes Occurring in men
- Metastatic theory:
Retrograde menstrual flow through Fallopian tubes -> explains ovarian and abdominal cavity spreading.
Hematogenous / lymphatic dissemination -> endometriosis appears in lungs / lymph nodes
Iatrogenic - surgeon moves it there accidentally -> explains abdominal laparotomy scars with it
- Metaplastic theory - multipotent stem cells become endometrium -> explains occurrence rarely in men
How can endometriosis appear grossly in the ovaries, serosa of pelvis / abdomen, and intestines?
Ovaries - “chocolate cysts” - blood-filled endometrioma
Serosa - “powder burns” - black spots on serosa
Intestines - induce fibrosis leading to adhesions and even mural-thickening of smooth muscle (Crohn’s like presentation)
How does endometriosis appear different than adenocarcinoma histologically?
There is proliferation of both the glands and the stroma
In endometrial adenocarcinoma -> Just the glands are proliferating
How can endometriosis cause infertility?
Causes fibrosis and scarring of the Fallopian tube -> impaired migration of sperm / egg + increased risk for ectopic pregnancy.
What is adenomyosis and how does it present?
Extension of the endometrial tissue into the uterine myometrium (overgrowth of basal layer into myometrium)
-> can be thought of as a local form of endometriosis
Presents with dysmenorrhea (painful menses with cramping), and menorrhagia (increased bleeding, like hemorrhage). Classically presents with uniformly enlarged uterus.
What cancer does endometriosis increase your risk of?
Ovarian carcinomas in a particular.
Endometrioid surface cell ovarian carcinoma often arises in this setting.
What proliferates in endometrial hyperplasia and what is the general underlying cause? How does it present?
Caused by a hyperplasia of endometrial GLANDS relative to stroma
Excess estrogen stimulation, i.e. obesity, estrogen replacement, anovulatory cycles, or polycystic ovarian syndrome (increased circulating estrone)
Presents as POSTmenopausal uterine bleeding
**Note that obesity is a key example because it allows for unopposed estrogen -> increased estrone without any progesterone due to lack of ovulation.
What does endometrial hyperplasia increased your risk for and what gene is associated with it?
Associated with inactivation of PTEN tumor suppressor gene
-> increased risk for endometrial carcinoma (endometroid type)
What are the two ways in which endometrial hyperplasia is histologically characterized based on its growth? Which is more important?
- Simple vs complex
- > simple = glands look nice
- > complex = glands look complicated with many outpouchings and loss of stroma - Presence of absence of cellular atypia
- > nuclear atypia is more important
What is the most common invasive tumor of the female genital tract? Which subtype is most common and who tends to get it?
Endometrial carcinoma
Endometrioid subtype is most common (80% of endometrial cancers), tends to be estrogen-related, happens in perimenopausal women (around 60 years)
What are the general risk factors which lead to greater estrogen factor throughout life? This includes risk factors for endometrial cancers, breast cancers, etc.
- Early menarche / late menopause - longer lifespan exposed to estrogen
- Nulliparity - having no kids prolongs your estrogen exposure throughout life b/c you don’t have estrogenfree period after birth
- Anovulatory cycles - prolonged estrogen exposure
- Obesity - increased estrogen conversion
Give one additional risk factor for endometrial carcinoma other than prolonged estrogen exposure.
Lynch syndrome -> typically causes endometrioid type endometrial cancer (microsatellite instabilities and PTEN mutations are seen in this type)
What is the other type of endometrial cancer and who tends to get it? Prognosis?
Sporadic endometrial cancer -> Type 2, occurs in older (wayyyy postmenopausal women, i.e. 70s/80s), no associated with estrogen
-> Occurs in the setting of atrophic endometrium with no precursor lesion
Associated with early p53 mutations and very aggressive behavior, invading myometrium
What is the most common form of sporadic endometrial carcinoma (Type 2) and what is seen on histology?
Serous endometrial carcinoma. Forms papillary structures which can necrose around fibrovascular cores, leading to psammoma body formation.
To remember it forms psammoma bodies, alot of people remember it as “papillary-serous endometrial carcinoma”
What causes fibroids and how will they change with age?
They are estrogen sensitive: tumor increases in size with pregnancy and decreases in size with menopause.
Peak occurrence is in 20-40 years.
How is a leiomyoma told apart from a leiomyosarcoma grossly?
Leiomyoma -> appears as a well-defined white, whorled mass with no hemorrhage or necrosis, and there are usually MULTIPLE
Leiomyosarcoma -> appears as a SINGLE lesion with areas of necrosis and hemorrhage
What are classic symptoms for leiomyoma?
Usually ASYMPOMATIC, but may present with abnormal uterine bleeding (stretch lining of uterus) with iron deficiency anemia, infertility (block ability of ovum to implant in wall), and a pelvic mass
Who tends to get leiomyosarcoma and how do they arise?
POSTmenopausal women
Arise de novo (NOT from a leiomyoma)
What are corpus luteum cysts and are they functional? What’s on the ddx?
Corpus luteum with blood in them which have a delayed resolution -> taking forever to turn into corpus albicans
-> also called a hemorrhagic luteal cyst by pathoma
DDx: Chocolate cyst from endometriosis
What are follicular cysts?
According to Bosch and Dr. Sattar, they are cysts formed by the slowness of degeneration of Graafian follicules post-rupture. They are common and have no clinical significance. First aid says these are unruptured follicles which may be functional and produce estrogen.
What is going wrong hormonally in PCOS which accounts for the symptoms?
Hyperinsulinemia / insulin resistance alter the hypothalamic hormonal balance and cause:
- Increased LH:FSH ratio, which stimulates increased androgen production from theca interna cells –> hirsutism.
- High circulating androgen levels are converted to estrone via adipose tissue (these women are obese with insulin resistance) -> feedback by estrone decreases FSH levels secreted by anterior pituitary.
- Since FSH is low, androgens are not rapidly turned into estrogen via granulosa cells -> slowed rate of follicular maturation. This leads to small follicular cysts and anovulation -> infertility.
What is the classic presentation of someone with PCOS then?
An obese young woman (adipose tissue required to make estrogen) with infertility, oligomenorrhea, hirsutism/hyperandrogenism, and often insulin resistance (obese)
What two conditions are you at increased risk of developing in the future due to PCOS?
- Type 2 diabetes - insulin resistance
- Endometrial cancer - due to unopposed circulating estrone and estrogen from anovulatory cycles -> corpus luteum is never made.
What is the treatment algorithm for PCOS?
- Weight reduction
- OCPs -> prevent endometrial hyperplasia due to unopposed estrogen (provide hormones exogenously)
- Clomiphene - infertility treatment which blocks estrogen receptor negative feedback in hypothalamus
- Metformin - to combat insulin resistance & helps ovulation
- Spironolactone / ketoconazole -> block androgen receptor as well as production
What are the three broad types of ovarian neoplasms and which is the most common?
- Surface epithelial tumors - most common - formed from coelomic epithelium
- Germ cell tumors
- Sex cord-stromal tumors
What are the three major histologic subclassifications of surface epithelial tumors of the ovary? Which is most common? What are they differentiated towards?
- Serous neoplasms - most common - differentiated towards fallopian tube
- Mucinous neoplasms - differentiated towards endocervix (keeps the sperm out with mucin) / intestinal mucus epithelium
- Endometrioid neoplasms - differentiated towards endometrium
What is the most common malignant ovarian neoplasm overall? What is the differentiation towards? What does it look like histologically?
Papillary serous cystadenocarcinoma -> papillary pattern means it’s differentiated towards Fallopian tube
Columnar epithelial cells, and since it is papillary carcinoma -> psammoma bodies are frequently seen
What are the three forms in which each subtype of ovarian neoplasm can be found?
- Adenoma - benign -> minimal epithelial proliferation
- Borderline - inbetween benign and malignant (malignant, but much better prognosis)
- Adenocarcinoma - marked epithelial proliferation and STROMAL INVASION
What are two gross features you look at to differentiate between benign and malignant ovarian neoplasms?
Solid areas -> more solid areas = more likely to be malignant. (More cystic = likely benign)
Bilateral = more likely malignant than benign
Who tends to get benign vs malignant surface epithelial ovarian tumors in terms of age?
Benign - usually in premenopausal women - aged 30-40
-> usually cystadenomas
Malignant - usually in postmenopausal women - aged 60-70s
-> usually cystadenocarcinomas
What gynecologic malignancies are BRCA1 patients at increased susceptibility for?
Serous tumors (i.e. cystadenocarcinomas) of the ovarian surface epithelium and fallopian tubes -> need to remove ovaries and fallopian tubes
What type of ovarian cancer arises in the setting of endometrial cancer and are they related?
Ovarian endometrioid carcinoma
-> often arises in the setting of endometriosis, but the uterine endometrial cancer is independent (not a metastasis of the same tumor)
What is pseudomyxoma peritonei and what is likely to cause it?
Mucinous material from ovarian tumor leaks into abdomen and causes mucinous ascites
Mucinous cystadenocarcinomas are most likely to cause it, can also be due to mucinous appendiceal tumor (Dr. Sattar has it in as a mucinous metastasis to the ovary)
What is a Brenner tumor and why is it unique?
It is a Benign tumor that is actually solid (rather than cystic) and is composed of Bladder epithelium (urothelial / transitional type)
What is the tumor marker for most ovarian surface neoplasms?
CA-125
How do ovarian adenocarcinomas typically disseminate?
Disseminate locally and have massive peritoneal involvement
-> present with ascites
May also disseminate in lymphatics or even hematogenously
-> poor prognosis
What is the most common germ cell tumor of females, what age group tends to get them, and where do they arise?
Mature cystic teratomas (benign)
Tend to occur in younger age group than benign surface epithelial tumors -> ages 10-30
Often arise in the ovary, but can arise anywhere along line of migration of germ cells (along the midline)
What is struma ovarii an example of and how does it present?
A monodermal teratoma which is mostly composed of mature thyroid tissue -> benign variant, but presents clinically as hyperthyroidism
If a mature teratoma becomes malignant, how does this usually happen? Are these tumors often bilateral?
Usually occurs due to a squamous cell carcinoma arising within the mature tissue (due to it being mostly ectodermal)
Actually yeah, they can be bilateral up to 10% of the time
What germ layer most commonly predominates in IMMATURE teratoma, and is it benign or malignant? What is seen histologically?
Neuroectodermal derived -> contains immature fetal tissue. (vs mature teratomas usually have surface ectoderm)
It is an aggressive malignancy typically, and is embryonal tissue intermixed with necrosis and hemorrhage
What is the most common MALIGNANT ovarian germ cell tumor? How do the cells appear?
Dysgerminoma (analogous to seminoma in males)
Cells appear large with clear cytoplasm and central nuclei (resembling oocytes or friend eggs)
What are the useful tumor markers in dysgerminoma and what is the prognosis?
Lactate dehydrogenase (LDH) is most useful.
hCG is also sometimes useful if syncytiotrophoblasts are intermixed
Excellent prognosis with radiation to chemotherapy (similar to seminoma, completely opposite to non-seminoma germ cell tumors)
What does histology of yolk sac tumor show and what is the serum marker?
Schiller-Duval bodies (glomeruloids structures) -> remember these are the “endodermal sinus”
-> alpha-fetoprotein is tumor marker (yolk sac)
What aggressive germ cell malignancy is often mixed with other types? What is its histologic pattern?
Embryonal carcinoma
-> Solid sheets and nests of large, pleomorphic cells, often making a pseudoglandular pattern
What is the tumor marker and prognosis of nongestational choriocarcinoma? What will be seen histologically?
Tumor marker is beta-HCG
Invasive cytotrophoblasts / syncytiotrophoblasts, but villi are ABSENT (unlike invasive mole)
Prognosis is god awful with early hematogenous spread (does not respond well unlike gestational choriocarcinoma)
What are sex cords vs stroma in “sex cord-stromal” tumors?
Derivative of:
1. Sex cords -> granulosa or Sertoli cells
- Stroma -> fibroblasts, theca cells, Leydig cells
If sexcord-stromal tumors are functioning, who tends to get estrogenic vs androgenic versions?
Androgenic - younger women
-> defeminization / virilization in a younger woman
Estrogenic - older women
-> abnormal uterine bleeding in an older adult
Obv there are exceptions
What is the most common malignant sex cord-stromal tumor? Who tends to get it gets it? What is their presentation?
Granulosa cell tumors
- > estrogen-secreting, thus adult-type (women in their 50s, postmenopausal)
- > presents as abnormal uterine bleeding due to endometrial hyperplasia
What can happen if granulosa cell tumors occur in pre-adolescents? What tumor marker is used to track it? What is seen histologically
Sexual precocity
Tumor marker is INHIBIN B -> made by granuloma cells to inhibit FSH
Call-Exner bodies
- > granulosa cells arranged around collections of eosinophilic material
- > follicular pattern which resembles primordial follicles (they think they are around germ cells)
What is a fibroma-thecoma and who tends to get it? What hormone is secreted?
Benign tumor of varying amounts of fibroblasts and theca cells (epithelial derived) -> actually produce estrogen (rather than testosterone, they go the next step). It’s actually the theca cells which are making estrogen.
Thus, like granulosa cell tumors, presents as abnormal uterine bleeding in postmenopausal women
What is Meigs syndrome? What might you confuse it for?
Triad of ovarian FIBROMA, ascites, and hydrothorax (pleural effusion)
-> might confuse for ovarian carcinoma ascites, but actually fibromas / thecomas are benign
What is the androgenic sex cord-stromal neoplasm which usually occurs in younger women? What does it look like histologically?
Sertoli-Leydig cell tumor (yes! this can occur in the ovaries!). Think this is the androgenic one because it would be normal in men!!!!!!
Sertoli cells will form tubes, and the Leydig cells will be the stroma between the tubules.
Reinke crystals can be seen on histology in Leydig cells (as in male Leydig cell tumors)
Think of Reinke Le-Digger!
What is a Krukenberg tumor? How can you differentiate this from primary ovarian malignancy?
Mucinous, signet-ring cell adenocarcinoma which has metastasized to ovary
-> usually due to diffuse gastric adenocarcinoma
-> typically metastases will be bilateral, whereas primary mucinous cystadenocarcinoma is unilateral usually
What is the most important test to run on a female who comes in with acute lower abdominal pain?
Pregnancy test -> ectopic pregnancy is a surgical emergency.
Give two common causes of ectopic pregnancy?
- Endometriosis - scarring of endometrium
2. Pelvic inflammatory disease - scarring of endometrium
What does placenta previa mean?
Placenta comes before baby
-> placenta is implanted in maternal uterine segment, sometimes overlying internal cervical os
What are the complications of placenta previa and what should be done about it?
Can lead to significant maternal hemorrhage since the placenta is directly over the opening to the vagina, and the decidua is not well-formed in this area.
Baby should be delivered by C-section to prevent fatal maternal hemorrhage during delivery
What are the risk factors for placenta accreta/increta/percreta?
- Prior C-section -> heals with scar tissue, and collagen cannot decidualize in response to hormones
- Uterine anomalies - leading to abnormal decidualization
- Placenta previa - lower uterus is not as hormone responsive as upper body -> improper decidualization
What are the potential complications of placenta accreta/increta/percreta?
- Retained placenta -> hard to get the placenta lose since it will be very adherent
- Retained placenta will cause post-partum hemorrhage and possible uterine rupture
- > significant bleeding, can lead to Sheehan syndrome / pituitary apoplexy
What is the clinical presentation of placental abruption for the mother?
Abdominal pain / tenderness in the third trimester marked by:
- Painful vaginal bleeding
- Uterine contractions
- Disseminated intravascular coagulation and hypovolemic shock -> placenta releases procoagulant factors
- > more likely to present with HTN than amniotic fluid emboli
What are the risk factors for placental abruption?
- Hypertension / preeclampsia - leads to poor placental disc perfusion
- Cocaine / nicotine use - poor perfusion due to vasocontriction
- Abdominal trauma
What is the definition of pre-eclampsia?
Development of hypertension, edema, and proteinuria during pregnancy, which may cause end-organ dysfunction
What are the severe symptoms of end-organ dysfunction in pre-eclampsia?
Headaches and visual disturbances secondary to hypertension, with hypercoagulability and acute kidney injury (due to fluid loss).
Pulmonary edema may result from proteinuria.
What is the proposed pathogenesis of pre-eclampsia?
Inadequate extravillous trophoblast remodeling of maternal spiral arteries leads to placental factors are released into circulation and cause diffusion endothelial dysfunction:
- > Vasoconstriction (damaged endothelium releases less NO)
- > Increased vascular permeability leading to edema / proteinuria
- > hypercoagulability due to endothelial damage
What are eclampsia and HELLP syndrome?
Eclampsia - Preeclampsia + seizures
HELLP - Severe pre-eclampsia leading to
- > Hemolysis, Elevated Liver Enzymes, Low Platelets
- > microangiopathic hemolytic anemia involving liver damage (lack of blood flow as thrombi form in sinusoids, shear RBCs into schistocytes, and then stop blood flow thru those areas)
How does molar pregnancy usually present / what is the usual way you know it’s happening?
Usually presents as spontaneous miscarriage or with increased uterine size and hCG levels which are TOO HIGH for gestational age (trophoblastic proliferation)
-> increased hCG may lead to theca cell cysts, hyperthyroidism, and early pre-eclampsia
How is molar pregnancy dealt with and what are the risks associated with it? What condition are these more common in?
Endometrial curettage
-> monitor hCG for recurrence, as it may develop into:
- Invasive mole (more common in complete mole than partial)
- Gestational choriocarcinoma (complete mole only)
How does a choriocarcinoma differ from a invasive mole?
Choriocarcinoma - there will be NO chorionic villi. It an invasive mole, the chorionic villi are present.
What is the clinical presentation of a choriocarcinoma?
uterine bleeding and elevated hCG levels.
Shortness of breath with hemoptysis is common due to early widespread dissemination hematogenously, including lungs, brain, liver, etc (trophoblasts are invasive).
How does gestational choriocarcinoma differ from germ cell choriocarcinoma?
They both look the same (malignancies of trophoblasts), but gestational-related choriocarcinomas have a far better prognosis, and respond well to chemotherapy.
Germ cell choriocarcinoma will probs kill you.
What are the key fetal effects of fetal alcohol syndrome?
Mental retardation
Also leads to facial abnormalities (i.e. smooth philtrum) and microcephaly
What are a couple important risk factors for SIDS? How is it best prevented?
Drug abuse in either parent (especially SMOKING), prone sleep position, sleeping with parents, over-swaddling / heat stress
Best prevented via keeping babies in SUPINE sleep position
How do OCPs modify your risk for ovarian cancer and why?
Reduce it. Exogenously providing hormones decreases FSH / LH release -> reduces the number of times ovulation occurs, and thus need for regeneration of ovarian surface epithelium.
How do you tell endometrial polyp and uterine fibroids (leiomyoma) apart?
Both cause cyclical having menstrual bleeding, especially if the uterine fibroids are superficial (submucosal) -> can cause ulceration and excessive bleeding.
Endometrial polyp -> will NOT distort the uterine shape
Fibroids -> will be palpable on bimanual exam #6432
