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297 Cards in this Set

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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.
FALSE
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).
sepsis
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
Klebsiella
Enterobacter
Enterococci
which three antibiotics should you never use to treat a UTI unless the UC shows the pathogen is susceptible?
Ampicillin
Amoxicillin
Sulfonamides
(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?
Quinolones
(oral or parenteral)
*high urinary concentrations*
optimal time period to treat acute uncomplicated cystitis?
3 days
3 treatments of choice for uncomplicated cystitis?
1. TMP/SMX
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?
*DO NOT TREAT UNLESS:*
- 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?
cephalosporin
nitrofurantoin
(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?
2wks
(unless is a cipro - then 7 days)
outpatient first line treatment for uncomplicated pyelonephritis?
FQ
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?
TMP/SMX
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?
~25%
(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?
acyclovir
valacyclovir
famcyclovir
(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?
7-10d
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?
(manifestations?)
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)
-or-
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)
PLUS
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)?
FQs
what would we use instead to treat gonorrhea infections acquired in Asia, Hawaii, California or MSM?
ceftriaxone
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?
Yes
in a BV infection do you treat the partner?
No
two antibiotics used to treat BV?
metronidazole (oral or intravaginal)
-or-
clindamycin (intravaginal)
topical therapy for vulvovaginal candidiasis? (2)
azoles
nystatin
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?
benign
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
stroma
hemosiderin laden macrophages
endometriosis
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
delivery
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
adhesions
(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?
tuberculosis
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)
endometriosis
leiomyomas
peritubal adhesion
IUDs?
in which portion of the uterine tube does an ectopic pregnancy MC occur?
ampulla
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?
lithopedion
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?
adenocarcinoma
(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?
4
the corpus luteum is under control of which hormone?
LH
what is the major estrogen in a menopausal woman? why?
estrone
(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?
ovary
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?
salpingitis
(this could result in a tuboovarian abscess)
in a patient with chronic oophoritis, the cause could very likely be _____ related.
autoimmune
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?
nonfunctional
is a follicle cyst of the ovary functional or nonfunctional?
functional
(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:
pregnancy
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?
endometrial
cervix
ovarian
what is the deadliest gynecologic malignancy?
ovarian
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)
breast
colon
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?
benign
gross characteristics of a mucinous cystadenoma?
multiloculated
large
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?
malignant
endometrioid carcinoma is usally found with which concurrent cancer?
endometrial adenocarcinomas
are ovarian clear cell adenocarcinomas benign or malignant?
malignant
are most ovarian clear cell adenocarcinomas unilateral or bilateral?
unilateral (90%)
are most Brenner cell tumors benign or malignant?
benign
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?
teratoma
are most germ cell tumors benign or malignant?
benign
a germ cell tumor that is derived from neoplastic germ cells is called?
dysgerminoma
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?
neuroectoderm
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)?
carcinoid
what is the following tumor called?
the female "counterpart" of testicular seminoma?
dysgerminoma
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?
RADIOSENSITIVE
(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.
feminizing
(secondary sex characteristics)
which tumor is associated with Meig's syndrome?
thecoma-fibroma
what is Meig's syndrome? (3 manifestations)
ovarian tumor
ascites
hydrothorax
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?
masculinization
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?
benign
are most tumors that are unclassified benign or malignant?
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?
80%
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?
funisitis
when villitis is present and you see granulomas under the scope, what is the most likely causative organism?
Listeria
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?
pre-eclampsia
eclampsia
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?
(4)
"vasospastic changes"
- placenta becomes ischemic
- fetal hypoxia
- oligohydramnios
- dysmaturity
results of pre-eclampsia/eclampsia on mother?
*arterial hypertension leads to:
- endothelial injury
- DIC
- 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?
CMV
what type of virus is CMV?
herpesvirus
describe the genome of CMV
large
linear
dsDNA
where does CMV establish a latent infection?
in lymphocytes and epithelial cells
what is the primary principle contributing to the virulence of CMV?
CMV proteins downregulate cell surface display of HLA complexes. This prevents CTL recognition of infected cells.
compare when women are seropositive for CMV in:
1. low SES
2. "affluent" communities
1. acquired at early age (80% seropositive by childbearing age)
2. acquired later (40-60% susceptible to CMV at reproductive age)
two mechanisms of vertical transmission of CMV?
1. transplacentally
2. during birth
how can CMV be acquired postnatally?
the infant ingests CMV positive breastmilk.
which CMV infection is more severe: prenatal or postnatal?
Prenatal
common manifestation of CMV in AIDS patients?
CMV retinitis
common manifestation of CMV following a bone transplant?
CMV pneumonitis
severe complication of CMV?
cytomegalic inclusion disease (CID)
*severe*
3 clinical manifestations in an infant of CID?
petechiae
hepatosplenomegaly
jaundice
4 possible complications of CID?
microcephaly
intracranial calcification
hearing loss
intrauterine growth retardation
hallmark sequelae of subclinical in utero CMV infection?
deafness
how do you differentiate CMV from EBV in a postnatal CMV infection?
CMV - heterophile negative infectious mononucleosis
EBV - heterophile positive infectious mononucleosis
which is more severe:
a congenital CMV infection acquired during maternal primary infection
-or-
a congential CMV infection acquired during a maternal secondary infection?
a congenital CMV infection acquired during a maternal primary infection
what is the "gold standard" test for diagnosing CMV?
PCR
histopathologic characteristics of CMV?
Owl's eye inclusions and marginated chromatin
drugs approved to treat CMV infection? (4)
1. cidofovir
2. foscarnet
3. valgancyclovir
4. gancyclovir
why does acyclovir not work on a CMV infection?
CMV lacks a TK gene, (therefore cannot phosphorylate acyclovir like it needs to be phosphorylated for activation).
are there any benefits to administering gancyclovir postnatally?
evidence has shown it reduces incidence of retardation and other sequelae
what is a rare complication of an in utero viral infection that results in death?
hemorrhagic complications
(DIC)
what class of viruses does varicella zoster belong to?
herpes viruses
where does varicella zoster establish latency?
in the dorsal root ganglia
how is VZV spread?
direct contact
airborne
what are two siginificant outcomes of a VZV infection during pregnancy?
1. congenital varicella syndrome (CVS)
2. neonatal varicella (worse)
when must VZV be contracted to possibly cause fetal abnormalities?
in the first or second trimester
top 5 congenital abnormalities seen in VZV?
skin scars
eye abnormalities
abnormal limb
premature/low birth weight
cortical atrophy/MR
how is neonatal varicella contracted from the mother?
contracted during the last two weeks of gestation (symptoms may not be present in the mother at time of birth)
what is a common visceral complication of neonatal varicella?
viral pneumonia
(fatal in 1/3 of cases)
treatment for neonatal VZV or newborns at risk for it?
immunoglobulin to VZV
(reduces severity of disease)
regarding HSV: which is more likely to be transmitted: a maternal primary or a maternal reactivated infection?
maternal primary infection (10x more likely)
is HSV acquired in utero?
rarely
more commonly acquired during birth or postnatally.
when do HSV symptoms typically appear in the newborn?
first 6 wks of life
(may manifest in first week - associated with worse outcome)
what three disease categories can newborns with HSV be divided into?
1. SEM (skin, eye, mouth)
2. CNS (encephalitis)
3. Disseminated (most severe)
how can a disseminated HSV infection be distinguished from sepsis?
in HSV see:
vesicular lesions
hepatitis
DIC
treatment/prevention of HSV?
1. C-section for women with active lesions at time of delivery
2. prophylactic acyclovir
3. infants - IV acyclovir
what class of virus does rubella belong to?
togavirus (enveloped viruses)
describe the rubella genome
(+) ssRNA
enveloped
is rubella a hardy virus?
NO!
heat-labile, sensitive to detergents, solvents, UV light, pH extremes
how many serotypes of Rubella are there?
one
(therefore easy to make an effective vaccine)
transmission of Rubella?
respiratory droplets
close personal contact
at what time in the pregnancy is the risk of congenital rubella syndrome (CRS) highest?
before 11 wks
describe the pathogenesis of a postnatal rubella infection
* virus enters via respiratory tract, infects respiratory epithelium
* spreads to lymph nodes
* replicates in nasopharynx and lymph nodes
* causes viremia
when is maximal transmission of the rubella virus in relation to appearance of the rash?
maximal transmission = 5 days before to 6 days after rash appears
where does replication of rubella occur in the fetus?
in virtually every organ
what exactly are the effects of CRS on fetal development thought to be due to? (4)
mitotic arrest
tissue necrosis
interference with blood supply
chromosomal damage
which serological marker would we look for in the mom that would indicate a primary infection?
IgM to rubella
a rubella IgM presence in early infancy (<6 mo) is indicative of?
a congenital rubella infection
could you give a pregnant woman an MMR?
NO!
it is a live attenuated vaccine!
Never give a pregnant woman a live attenuated vaccine...