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297 Cards in this Set
- Front
- Back
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 |
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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 |
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what are some endocrine factors that could result in spontaneous abortion? (3)
|
1. Luteal phase defect (decreased progesterone synthesis)
2. Thyroid disease 3. hyperandrogenism |
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paternal factors increasing risk of a spontaneous abortion? (2)
|
1. chromosomal abnormalities
2. advanced age of sperm |
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which two things, if they happen in the first trimester of pregnancy, result in an inevitable abortion?
|
1. rupture of membranes
2. cervical dilation |
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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
|
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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 |
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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... |