This lady had preterm premature rupture of membranes. She had a genital tract infection, which is a risk factor for PPROM.
From Uptodate:
Many of the microorganisms that colonize the lower genital tract have the capacity to produce phospholipases, which can stimulate the production of prostaglandins and thereby lead to the onset of uterine contractions. In addition, the host's immune response to bacterial invasion of the endocervix and/or fetal membranes leads to the production of multiple inflammatory mediators that can cause localized weakening of the fetal membranes and result in PPROM.
cheesetouchsome institutions give students UpToDate access+6
cbrelandI knew that misoprostol (PGE1) can be used for abortions by forcing uterine contractions, so I figured the answer had something to do with prostaglandins+11
rthavranekI knew prostaglandins increased uterine contraction, but I also thought PGE2 caused cervical ripening and since there was a closed cervix, I eliminated that choice. I had no idea what was going on so I just picked oxytocin since that would increase uterine tone without dilation, though my reasoning seems to be incorrect+2
notyasupremeI think also it said that the fetus releases oxytocin and steroids, which I guess is stupid wording that makes it not right. Anyways, fuck the curve on NBME 18 :) +4
okokok1if anyone didn't know what "PPROM" stood for it is: Preterm Premature Rupture Of Membranes"+4
aakbI was between the prostaglandin answer and stressed fetal production and release of oxytocin and the reason I didn't pick oxytocin was if the cervical os is closed (membranes ruptured 32 hrs ago and contractions been going on for 12) and there's no effacement, it didn't seem like that baby actually wanted to come out so I thought that's not what's happening here. Plus mom has a fever so inflamed maternal decidua seemed to fit. +2
helpplsIf there was an increase in Pgs why did she not have a ripened cervix? +
leemaxread it again guys-option E-stressed fetal production and release of OXYTOCIN.
good nbme,got me there!+1
gabriellerenaiI think a key thing is that oxytocin is never the primary initiator of labor even in full term labor (it mainly controls Phase 3 and 4): via up to date - "It is unlikely that oxytocin provides the trigger for the initiation of labor, but the release of oxytocin during labor results in more forceful uterine contractions and undoubtedly facilitates delivery of the fetus and placenta."+3
gabriellerenaiand their question was what is the primary stimulus+
epiglotitties@leemax doesn't the fetus produce oxytocin? and its clearly stressed, a fetal heart rate of 210 is high isnt it? Still don't get why that couldnt be the answer..+
fatboyslimI got this wrong and chose oxytocin. But now I recall a UW question saying oxytocin receptors on the uterus don't play much of a role in uterine contractions until about the late 3rd trimester. This fetus is 27 weeks gestation.+
submitted by โscrambledeggs(17)
This lady had preterm premature rupture of membranes. She had a genital tract infection, which is a risk factor for PPROM.
From Uptodate: Many of the microorganisms that colonize the lower genital tract have the capacity to produce phospholipases, which can stimulate the production of prostaglandins and thereby lead to the onset of uterine contractions. In addition, the host's immune response to bacterial invasion of the endocervix and/or fetal membranes leads to the production of multiple inflammatory mediators that can cause localized weakening of the fetal membranes and result in PPROM.