Glossary of Block VII, WeekV

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define an uncomplicated UTI.
cystitis in a nonpregnant woman without an underlying anatomic abnormality or neurologic dysfunction.
T/F: a male can have an uncomplicated UTI.
every UTI in a male is complicated
pharmacologically, what are the treatment implications of a complicated UTI vs. an uncomplicated UTI?
uncomplicated - low risk for treatment failure
complicated - increased risk for treatment failure
what type of pathogenic organism, causing a UTI, would place this UTI in the "complicated" category?
urease producing organism
(ie. Proteus mirabalis)
in diagnosing a UTI - what would a positive nitrite test tell us about the causative organism?
tells us it is gram negative
(gram negative organisms convert nitrate to nitrite)
what is a frequent complication of UTIs (as a matter of fact UTIs are the #1 cause of this complication).
what is the regular "cutoff" in a UC, where, above it, a UTI is diagnosed?
10^5 bacteria/mL
which pathogens cause most uncomplicated UTIs?
E. coli
S. saprophyticus
(minor: Enterococci, Klebsierlla, P.mirabolis)
which pathogens cause most complicated UTIs? (6)
E. coli
P. mirabolis
P. aeruginosa
which three antibiotics should you never use to treat a UTI unless the UC shows the pathogen is susceptible?
(high rates of resistance)
which urinary analgesic agent reduces symptoms of dysuria and colors the urine red/orange?
phenazopyridine HCL (pyridium)
which antibiotic is the one of choice in the treatment of complicated UTIs and areas of increased resistance?
(oral or parenteral)
*high urinary concentrations*
optimal time period to treat acute uncomplicated cystitis?
3 days
3 treatments of choice for uncomplicated cystitis?
2. TMP
3. Quinolones
what 3 conditions must be met before you use TMP/SMX in uncomplicated cystitis?
1. no allergy
2. not recently received antibiotics
3. local resistance <15-20%
treatment indications for asymptomatic bacteriuria?
- child
- pregnant
- before urologic surgery
why are pregnant women treated for asymptomatic bacteriuria (UC>10^5)?
they have:
- a 20x increased risk of pyelonephritis
- an increased risk of stillbirth or premature labor
what would we use to treat a pregnant woman with asymptomatic bacteriuria?
(NOT quinolones!)
why would you not use a urinary antiseptic to treat pyelonephritis?
poor tissue concentration
List three urinary antiseptics
1. nitrofurantoin
2. methenamine
3. fosfomycin
spectrum of nitrofurantoin?
basically all urinary pathogens EXCEPT Pseudomonas, Proteus, Serratia
indications for nitrofurantoin? (2)
1. uncomplicated cystitis
2. prophylaxis of recurrent cystitis
hallmark side effect of nitrofurantoin?
pulmonary fibrosis
(may not be reversible)
if therapy for cystitis fails, how should we treat the infection?
as if it is pyelonephritis
(silent pyelo occurs in ~30% of cystitis cases)
what is the duration of antibiotic therapy for pyelonephritis?
(unless is a cipro - then 7 days)
outpatient first line treatment for uncomplicated pyelonephritis?
outpatient treatment for pyelonephritis when a gram + organism (ie. Enterococcus) is suspected?
amoxicillin or amox/clavulanate
inpatient treatment for uncomplicated pyelonephritis?
IV FQ, aminoglycoside, 3rd gen. ceph
inpatient treatment for pyelonephritis when a gram + organism (ie. Enterococci) is suspected?
Amp/sulbactam or ampicillin + aminoglycoside
what is the most commonly used medication in the prevention of recurrent UTIs?
what type of patients would be on long-term, low-dose prophylaxis for recurrent UTIs?
Pediatric population
Pregnant women
Elderly population
what is the ~ seroprevalence for HSV-2?
(many don't know they are infected)
what is the difference in symptoms seen between a primary and a secondary HSV infection?
primary - both local and systemic symptoms
secondary - mostly local symptoms, milder
How long does HSV remain latent and where does it establish latency?
remains latent indefinitely in neuronal bodies
in a recurrent HSV infection, when should antiviral treatment be initiated?
at the onset of prodromal symptoms
(tingling, irritation, pain in buttocks, legs or hips)
compare the number of lesions seen in a primary vs. a secondary HSV infection.
primary - 16 lesions on avg.
secondary - 6 on avg.
which antivirals are effective in treating HSV?
(equal efficacy)
describe the effects of antiviral treatment on establishing latency in HSV.
NO effects in establishing latency of HSV
length of treatment time with acyclovir in primary HSV?
compare the initiation times of antiviral treatment in a primary vs. secondary HSV infection
primary - within 48-72 hours of onset
secondary - within 24 hours of lesions
duration of antiviral treatment of secondary HSV infection?
3-5 days
benefits of daily HSV suppressive therapy? (3)
1. decreases recurrences
2. decreases viral shedding
3. reduces risk of infecting uninfected partners
indications for daily HSV suppressive therapy? (3)
1. frequent or severe recurrences
2. HSV discordant couples
3. pregnancy
what is the drug of choice for the treatment of all stages of syphillis?
Benzathine penicillin G (IM)
what is the Jarisch-Herxheimer rxn?
self-limited reaction to anti-treponemal therapy
(fever, headache, myalgia, N/V, chills, exacerbation of secondary rash)
what two "syndromes" is Chlamydia trachomatis associated with?
1. Fitz-Hugh-Curtis syndrome (perihepatitis)
2. Reiter's syndrome (urethritis, conjunctivitis, arthritis, mucuocutaneous lesions)
what is the recommended treatment regimen for an uncomplicated Chlamydia infection?
azythromycin (single dose)
doxyxycline (BID for 7d)
Neisseria gonorrhoeae has demonstrated resistance to which two antibiotics?
1. penicillin
2. tetracyclines
what is the recommended regimen to treat an uncomplicated gonorrhea infection?
cefixime (single dose)
-(or ceftriaxone or FQ)
azithromycin or doxycycline (for Chlamydia tx.)
if Gonorrhea was acquired in Asia, Hawaii, California or MSM what could it be resistant to (therefore we should not use this to treat these infections)?
what would we use instead to treat gonorrhea infections acquired in Asia, Hawaii, California or MSM?
in a PID infection, what pathogen should we worry about that is particularly difficult to get rid of?
Bacteroides fragilis
two parenteral regimens to treat PID?
1. cefotetan (or cefoxitin) PLUS doxyxycline (for chlamydia)
2. clindamycin PLUS gentamycin PLUS doxycycline
two oral regimens to treat PID?
1. FQ W/ or W/O metronidazole
2. ceftriaxone PLUS doxy W/ or W/O metronidazole
which three STDs can be treated with a single dose antibiotic?
1. chlamydia
2. gonorrhea
3. trichomonas
which antibiotic is given in a single dose to treat trichomonas?
metronidazole (2g)
in trichomonas infection do you treat the partner?
in a BV infection do you treat the partner?
two antibiotics used to treat BV?
metronidazole (oral or intravaginal)
clindamycin (intravaginal)
topical therapy for vulvovaginal candidiasis? (2)
oral therapy for vulvovaginal candidiasis?
fluconazole (single dose)
two treatment regimens for HPV external warts?
1. podofilox
2. imiquimod
MOA of imiquimod?
immune response modifier
- enhances natural cellular immune mechanisms
- no anti-HPV activity
four provider administered regimens for external HPV warts?
1. cryotherapy
2. podphyllin resin
3. trichloroacetic acid (TCA)
4. surgical removal
describe what a crossection of uterine tube would look like in the:
1. interstitial portion
2. isthmus
3. ampulla/infundibulum
1. narrow lumen rimmed by muscle
2. decidualization, less cilia
3. lots of ciliated epithelium
gross manifestations of salpingitis isthmica nodosa?
nodual swelling of the isthmic portion of the uterine tubes
microscopic manifestations of sapingitis isthmica nodosa?
1. thickened wall
2. hypertrophied musculature
3. epithelium line channels running between muscle bundles (channels connect but do not extend to peritoneum)
Three postulated causes of salpingitis isthmica nodosa?
1. inflammation
2. mechanical pressure (diverticula)
3. analagous to adenomyosis
salpingitis isthmica nodosa is more commonly found in what two groups of women?
1. infertile ones
2. ectopic pregnancies
where does the typical peratubal cyst occur?
in the broad ligament
what three things may a peritiubal cyst be derived from?
1. mullerian ducts (paramesonephric)
2. wolffian ducts (mesonephric)
3. peritoneal inclusion (mesothelial)
what are hydatids of Morgagni?
little cysts found on the fimbriated portion of the uterine tubes and broad ligament
is an adenomatoid tumor of the uterine tube benign or malignant?
describe the microscopic characteristics of an adenomatoid tumor
cleft like spaces of mesothelial epithelium in loose stroma
which disorder can be present in the fallopian tubes and has the following microscopic characteristics?
endometrial glands
hemosiderin laden macrophages
s/s of acute salpingitis? (5)
1. pelvic pain
2. adnexal tenderness
3. pain with cervical motion
4. vaginal discharge
5. fever
possible complication of salpigitis?
destruction of tubal epithelium resulting in formation of a tubo-ovarian absess
"violin strings" (a complication of salpingitis) is also known as? and is?
aka. Fitz-Hugh curtis syndrome
*perihepatitis in female with a history of gonococcal or chlamydial salpingitis
besides STDs, what are some other causes of acute salpingitis?
infection after:
spontaneous/induced abortions
peurpural infections
(often polymicrobial)
describe the gross characteristics of acute salpingitis.
distended uterine tubes
early fibrinous adhesions
untreated acute salpingitis may progress to? which may progress to?
parametritis, which may progress to peritonitis
gross characteristics of pyosalpinx?
HUGE distended uterine tube
(pyosalpinx = pus bag)
four complications of PID?
1. peritonitis
2. intestinal obstruction
3. bacteremia/septicemia
4. infertility, ectopic pregnancy
more than 40% of women diagnosed with PID are in what age group?
15-24 yrs
minimum criteria for PID? (3)
1. lower abdominal tenderness
2. adnexal tenderness
3. cervical motion tenderness
besides STDs, what are some other causes of PID? (4)
1. appendicitis
2. diverticulitis
3. hematogenous spread
4. transuterine (IUD, D&C)
why is a ruptured tuboovarian abcess so emergent?
risk of gram negative endotoxic shock
what is hydrosalpinx?
collection of sterile fluid in the lumen of the uterine tubes
also see distended tubes
in a hydrosalpynx, what microscopic changes are seen in the uterine tube?
1. epithelium thin and nonciliated
2. thinned muscular wall, loss of plicae
hydrosalpynx is usually the sequelae to?
chronic salpingitis that has been treated or resolved
granulomatous salpingitis almost always has what origin?
via what 2 routes is fallopian tube tuberculosis spread?
hematogenous or lymphatic
fallopian tube tuberculosis is most commonly seen in what population?
immigrant population
3rd world countries
post-menopausal women (in US)
4 causes of ectopic pregnancy? (given to us by Torgerson)
peritubal adhesion
in which portion of the uterine tube does an ectopic pregnancy MC occur?
compare hCG levels in an ectopic pregnancy vs. a normal pregnancy
ectopic - lower hCG levels, don't see normal doubling rate
normal - see hCG double every 2 days
compare progesterone levels in an ectopic pregnancy vs. a normal pregnancy
ectopic pregnancy has lower progesterone levels
most ectopic pregnancies rupture at what time?
10-12 wks
what is it called when the ectopic pregnancy terminates in the uterine tube and just hangs out there?
malignant neoplasms of the uterine tube present in what age group of women?
6th-7th decades
clinical presentation of malignant neoplasms of the uterine tube? (3)
1. vaginal discharge/bleeding
2. pelvic pain
3. insidious onset of abdominal bloating/ascites
the majority of malignant uterine tube neoplasms are of what type?
(arise from uterine tube epithelium)
describe the spread of fallopian tube carcinoma
- transluminal into peritoneal cavity, implants on peritoneal surfaces
- direct invasion of uterus and ovary
- spread to lymph nodes
describe the four FIGO stages of fallopian tube carcinoma
0. carcinoma in situ
1. limited to uterine tube
2. pelvic extension
3. peritoneal/omental implants outside of pelvis / mets. to retroperitoneal lymph nodes
4. distant mets
which FIGO stages are considered incurable?
2, 3 and 4
(once it has spread)
describe the number of follicles in a female throughout life.
newborn - million, then some die off
puberty - less
reproductive years - 450 are ovulated
dissapear at menopause
embryology: what two things does the mesenchymal stroma give rise to?
theca and granulosa cells
describe the sequence from primordial follicle to Graafian follicle (5)
primordial follicle
primary follicle
early primary follicle
secondary follicle
Graafian follicle
if pregnant, how long does the corpus luteum secrete progesterone?
until the 3rd month
(then placenta takes over)
what maintains the corpus luteum of pregnancy? (ie. why doesn't it die like it does in an unfertilized cycle)
the developing embryo secretes hCG - this maintains CL.
what are the three components of the ovary?
1. epithelial surface
2. mesenchymal stroma
3. germ cells
at what developmental age do the germ cells of the ovary cease multiplying?
third trimester
ovarian arterial supply?
ovarian artery
(branch of abdominal aorta)
ovarian venous drainage?
drain into utero-ovarian vain
where do the lymphatics drain?
lumbar lymph nodes
describe the surface epithelium of the ovary?
single layer of columnar cuboidal cells
which type of cell in the ovary is responsive to hCG?
Hilus cells
about how many follicles are mature in each ovulation cycle?
the corpus luteum is under control of which hormone?
what is the major estrogen in a menopausal woman? why?
(no more follicular synthesis of estradiol)
a follicle cyst or a corpus luteum cyst can progress to ?
a hematoma
what is the MC site of endometriosis?
what is the cyst called that is seen in endometriosis?
chocolate cyst
(blood filled)
stromal hyperplasia and hyperthecosis results in bilateral ovarian enlargement. consequence?
stromal cells syntheslize androgens.
these androgens are converted peripherally to estrone, this leads to increased incidence of endometrial hyperplasia/carcinoma.
oophoritis is rare; often it is associated with concurrent inflammation of?
(this could result in a tuboovarian abscess)
in a patient with chronic oophoritis, the cause could very likely be _____ related.
what happens during ovarian torsion?
the ovary twists on its pedicle -> this results in congestion and infarction
is a serous inclusion cyst of the ovary functional or nonfunctional?
is a follicle cyst of the ovary functional or nonfunctional?
(high estrogen content in cyst fluid, also causes abnormalities in the release of pituitary gonadotropins)
what are the characteristics of a corpus luteum cyst?
- continued progesterone secretion (causes menstrual irregularities)
complications of an ovarian cyst?
intraperitoneal rupture
hemorrhage into cyst
what are the clinical features of PCOS?
1. obesity
2. hirsutism
3. secondary amenorrhea
4. infertility
what is the hormonal imbalance in PCOS?
excessive synthesis of androgens - these are converted peripherally to estrone
what hormonal imbalance are theca-leutein cysts associated with?
increased circulating gonadotropins
- causes stimulation of theca interna
- causes extensive cyst formation
what do all these conditions have in common:
hydatidiform mole
exogenous gonadotropin
high hCG levels
what three tissues of derivation can ovarian neoplasms arise from?
1. coelomic epithelium (mullerian or surface epithelium)
2. germ cells
3. stroma (sex cords)
seven neoplasms derived from coelomic (outer) epithelium?
1. serous tumors
2. mucinous tumors
3. endometrioid tumors
4. clear cell tumor
5. Brenner tumor
6. Carcinosarcoma
7. mixed mesodermal tumor
how are/were borderline ovarian tumors distinguished from frankly invasive epithelial cell tumors?
borderline tumors have no destructive infiltrative growth or stromal invasion
neoplasms derived from germ cells? (6)
1. teratoma
2. dysgerminoma
3. embryonal carcinoma
4. endodermal sinus tumor
5. choriocarcinoma
6. gonadoblastoma
four neoplasms derived from specialized gonadal stroma?
1. granulosa-theca cell tumors
2. Sertoli-Leydig tumors
3. Gynandroblastoma
4. Lipid cell tumors
two types of granulosa-theca cell tumors?
1. granulosa cell tumor
2. thecoma-fibroma
(derived from gonadal stroma)
two types of Sertoli-Leydig tumors?
1. arrhenoblastoma
2. sertoli cell tumor
5 neoplasm locations that commonly metastasize to the ovary?
1. GI tract (Kruckenberg)
2. Breast
3. Endometrium
4. Lymphoma
5. Lung
what are the top 3 gynecological malignancies?
what is the deadliest gynecologic malignancy?
why are ovarian tumors so deadly?
by the time they are discovered ~75% of them have spread to the pelvis and abdomen.
3 risk factors for ovarian CA?
1. nulliparity
2. family history (BRCA genes)
3. estrogen? (HRT)
effect of OCs on ovarian CA risk?
protective against ovarian CA
two features in molecular biology that predispose to ovarian CA?
1. High levels of HER2-neu
2. mutations in p53 tumor suppressor gene
if a patient has a BRCA1 or BRCA2 gene, what is their essential risk of ovarian CA?
20-60% by age 70
BRCA1 is highly expressed in what type of ovarian CA?
borderline ovarian carcinomas
BRCA2 is highly expressed in what type of ovarian carcinoma?
serous cystadenocarcinomas
presence of the BRCA gene also increases risk of what cancers? (besides ovarian)
four things that decrease the risk of ovarian CA?
1. breastfeeding
2. OCs
3. pregnancy
4. tubal ligation (and ovarian conservation)
clinical presentations of ovarian CA? (6)
1. increase in abdominal girth
2. urinary symptoms
3. ovarian torsion
4. ascites
5. functional endocrinopathies
6. abnormal uterine bleeding *(in about 1/3 of cases)*
3 tumor markers used in ovarian CA screening?
1. CA-125
2. hCG
3. alpha fetoprotein
tumors of this origin make up:
60-75% of primary ovarian tumors
90% of malignant ovarian tumors
surface epithelium
which type of epithelial ovarian tumor is the most common?
serous tumor
which type of epithelial ovarian tumor has the highest malignant potential?
serous tumor
what is the most common benign ovarian tumor?
serous cystadenoma
what is the malignant equivalent of a serous cystadenoma?
serous cystadenocarcinoma
which microscopic feature, when seen in serous cystadenocarcinoma, delivers a poor prognosis?
psammoma bodies
"tombstones of tumor cells"
are most mucinous tumors benign or malignant?
gross characteristics of a mucinous cystadenoma?
cysts filled with thick mucinous contents
classic micro characteristics of a mucinous adenocarcinoma?
"picket fence"
single epithelial cells line the cyst
what is pseudomyxoma peritonei and what is it associated with?
mucin errupts in to the peritoneal cavity eliciting a fibrous response (get adhesions and bowel obstruction)
*associated with mucinous carcinoma of the ovary or appendix
are most endometriod tumors benign or malignant?
endometrioid carcinoma is usally found with which concurrent cancer?
endometrial adenocarcinomas
are ovarian clear cell adenocarcinomas benign or malignant?
are most ovarian clear cell adenocarcinomas unilateral or bilateral?
unilateral (90%)
are most Brenner cell tumors benign or malignant?
characteristic micro of ovarian clear cell adenocarcinoma?
"hobnail" cells (clear cytoplasm)
*tubes or sheets of clear tubes*
what does a Brenner tumor resemble?
Bladder epithelium
which type of tumor accounts for >90% of all germ cell tumors?
are most germ cell tumors benign or malignant?
a germ cell tumor that is derived from neoplastic germ cells is called?
what is a teratoma derived from?
embryonic tissues
what tissues are endodermal sinus tumors and choriocarcinomas derived from?
extraembryonic tissues
what is another name for a benign cystic teratoma?
dermoid cyst
compare the nature of a mature teratoma vs. an immature teratoma
mature - benign
immature - malignant, rare
compare the nature of the cyst in a mature teratoma vs. an immature teratoma
mature - liquid-like cyst
immature - solid cyst
what is the part of the immature teratoma that is considered responsible for its agressive nature?
in what age group are immature teratomas most commonly seen?
first two decades
what is the following called?
a monodermal teratoma in which the predominant tissue is thyroid?
stroma ovarii
what is the following called?
a monodermal/specialized teratoma that produces carcinoid syndrome (where you must first exclude metastasis from the GI tract)?
what is the following tumor called?
the female "counterpart" of testicular seminoma?
two laboratory levels that would be elevated in a patient with dysgerminoma?
1. lactic dehydrogenase
2. hCG
unique feature of dysgerminomas when it comes to treatment?
(therefore good prognosis, respond to radiation treatment)
yolk sac tumors are MC present in which age group?
10-30 yrs
what do yolk sac tumors produce?
alpha fetoprotein
microscopic hallmark characteristics of a yolk sac tumor?
Schiller-Duval bodies
prognosis for yolk sac tumors?
used to be lethal
now most are cured with chemotherapy
embryonal carcinoma is associated with what elevated laboratory levels? (2)
elevated hCG
elevated alpha fetoprotien
choriocarcinoma is associated with what laboratory results?
elevated hCG
what is the most common ovarian tumor with estrogenic manifestations?
granulosa-theca cell tumor
micro hallmark characteristic of granulosa-theca cell tumors?
Call-Exner bodies
describe the manifestations of a granulosa-theca cell tumor in a child.
(secondary sex characteristics)
which tumor is associated with Meig's syndrome?
what is Meig's syndrome? (3 manifestations)
ovarian tumor
thecomas may be associated with what other type of gynecological change?
1. endometrial hyperplasia/carcinoma
2. granulosa cell tumor
why are fibromas unique when compared to the other ovarian stromal tumors?
it does not release estrogen, therefore no fat is present.
a luteoma is associated with what clinical presentation?
clinical features of a Sertoli-Leydig Cell tumor?
masculinize (hirsutism, male hair distribution, voice changes, clitoral hypertrophy)
defeminization (breast atrophy, amenorrhea, hair loss)
are Sertoli-Leydig cell tumors benign or malignant?
are most tumors that are unclassified benign or malignant?
a Kruckenberg tumor usually comes from?
the stomach
(characterized by signet ring cells)
three treatment modalities for ovarian cancer in general?
1. surgery with debulking
2. radiation
3. chemotherapy
what is the most common type of placental structure seen in twins?
dichorionic diamnionic (two separate ones)
when do most spontaneous abortions occur?
in the first 12 wks of pregnancy
risk factors for a spontanous abortion?
1. increasing maternal age
2. increasing parity
3. increasing paternal age
4. conception w/i 3 months of a live birth
50% of spontanous abortions are the result of chromosomal abnormalities. what is the chance of subsequent pregnancies having chromosomal abnormalities as well?
maternal infections that can result in spontaneous abortion?
T - Toxoplasmosis
O - Other (Listeria, mycoplasma hominis, ureaplasma urealyticum)
R - Rubella
C - Cytomegalovirus
H - not relevant to spontaneous abortion
what are some endocrine factors that could result in spontaneous abortion? (3)
1. Luteal phase defect (decreased progesterone synthesis)
2. Thyroid disease
3. hyperandrogenism
paternal factors increasing risk of a spontaneous abortion? (2)
1. chromosomal abnormalities
2. advanced age of sperm
which two things, if they happen in the first trimester of pregnancy, result in an inevitable abortion?
1. rupture of membranes
2. cervical dilation
what is the treatment for an incomplete abortion?
suction and curettage
what is a septic abortion?
complications of an incomplete abortion. manifests as sepsis, shock, hemorrhage, renal failure
what is the term for inflammation of the umbilical cord?
when villitis is present and you see granulomas under the scope, what is the most likely causative organism?
what is velamentous insertion of the umbilical cord?
trapping of the cord within the membranes
what placenta accreta?
when a defective decidual layer allows the placenta to attach directly to the myometrium. (results in hemorrhage after delivery)
what is placenta increta?
when the placenta penetrates the myometrium
what is placenta percreta?
when the placenta invades the myometrium and attaches to the peritoneal surface
(may result in rupture of the uterus)
what is placenta previa?
when the placenta implants in the lower uterine segment. this may occlude the cervical os.
(causes premature labor, bleeding as the cervix dilates)
what is abruptio placenta?
premature separation of the normally implanted placenta from the uterine wall
(results in fetal anoxia and maternal hemorrhage)
what constitutes HTN in pregnancy?
systolic >140 mmHg
diastolic > 90 mmHg
terms for pregnancy induced hypertension?
3 clinical s/s of pre-eclampsia?
1. HTN
2. proteinuria
3. edema
when is pre-eclampsia more common?
1. primigravida
2. extreme ends of reproductive years
what makes pre-eclampsia eclampsia?
presence of convulsions
What does the HELLP syndrome consist of?
H - Hemolysis
E - Elevated Liver enzymes
L - Low Platelets
describe the levels of the following in pre-eclampsia/eclampsia:
1. renin/angiotensin II
2. prostaglandins
3. thromboxane
4. endothelin
5. NO
1. increased
2. decreased
3. increased
4. increased
5. decreased
result of pre-eclampsia/eclampsia on fetus?
"vasospastic changes"
- placenta becomes ischemic
- fetal hypoxia
- oligohydramnios
- dysmaturity
results of pre-eclampsia/eclampsia on mother?
*arterial hypertension leads to:
- endothelial injury
- multi-system failure
describe gestational trophoblastic disease (GTD)
abnormal proliferation and maturation of trophoblastic tissue
MC manifestation of gestational trophoblastic disease?
hydatidiform mole
why are we worried about gestational trophoblastic disease (possible complication)?
malignant transformation
Why does GTD present clinically as a pregnancy?
elevated hCG
distended abdomen
what is the major difference between a complete and an incomplete hydatidiform mole?
complete - no fetus or fetal membranes associated with it
incomplete - presence of a chromosomally abnormal embryo or fetus
what "invades" what in an invasive hydatidiform mole?
villious trophoblast invades underlying myometrium
(can spread to distant sites)
gross appearance of a hydatidiform mole?
"cluster of grapes"
possible complication of hydatidiform mole?
progression to choriocarcinoma
(malignant tumor derived from trophoblast)
~1/140 molar pregnancies
via what route does choriocarcinoma spread?
invades the venous sinuses, then metastasizes to the:
lungs, brain, liver, vagina, GI tract
what laboratory value can be used to follow progression/remission of a choriocarcinoma?
hCG levels
(tumor produces hCG)
treatment for a choriocarcinoma?
aggressive tumor: treat with chemotherapy, hysterectomy, radiation
what exactly produces hGC?
syncitiotrophoblasts of the growing placenta
what is the most common congenital infection in the US?
what type of virus is CMV?
describe the genome of CMV
where does CMV establish a latent infection?
in lymphocytes and epithelial cells

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